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Microbiology > Lec 19: Host Microbe Interaction > Flashcards

Lec 19: Host Microbe Interaction Flashcards

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1
Q

what are two ways that we interact with microbes?

A

-transient exposures
and
-colonization

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2
Q

colonization can be what two types of relationships with our body?

A

parasitic and non-parasitic

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3
Q

when colonization is non-parasitic, what is that?

A

the normal microbiota

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4
Q

when colonization is parasitic, what is that?

A

an infection (harmful)

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5
Q

what two things can an infection be?

A

subclinical and infectious disease

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6
Q

what is a subclinical infection?

A

no symptoms infection

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7
Q

what is an infectious disease?

A

an infection that causes impairment of body function

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8
Q

what is colonization?

A

-The attachment and growth of a microbe on a surface.
when microbes can colonize with or on our body (attach, eat food, grow, and reproduce)

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9
Q

do minority or majority of microbes cause disease?

A

only minority of microbes cause diseases

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10
Q

what is an infection?

A

colonization by a harmful microbe (parasite) on or within our body

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11
Q

what is an infectious disease?

A

infection that prevents the body from functioning normally

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12
Q

what is a pathogen?

A

an organism or agent (virus; non-living) causing disease.
ex: SARS-CoV-2

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13
Q

what is a host?

A

an organism where a pathogen lives.
ex: humans and animals

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14
Q

what is pathogenicity?

A

the ability to cause disease

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15
Q

what is a pathogenic microbe?

A

causes disease

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16
Q

what is a non-pathogenic microbe?

A

does not cause disease

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17
Q

what is virulence?

A

the degree of pathogenicitiy

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18
Q

for virulence, what is the relationship between the disease severity and the pathogen virulence?

A

the higher the disease severity, the higher the pathogen virulence

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19
Q

what is etiology?

A

the cause of disease
ex: SARS-CoV-2 virus causes the disease COVID-19

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20
Q

what is a predisposing (risk) factor?

A

anything that makes the body more susceptible to disease

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21
Q

what is pathogenesis?

A

the course of a disease

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22
Q

what are three different types of pathogenesis?

A

-acute
-chronic
-latent

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23
Q

what is the acute pathogenesis and examples?

A

short-term illness, ex: flu, common cold, strep throat, COVID-19

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24
Q

what is an incubation period?

A

time from exposure to the pathogen to when the hosts start showing signs and symptoms of the disease

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25
Q

what is the acute incubation period signs and symptoms?

A

Signs: observable and measurable like fever, rash, and swelling.
Symptoms: subjective like tiring, pain, nausea

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26
Q

what is the acute illness?

A

time during which host displays signs and symptoms of disease

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27
Q

what is a convalescence?

A

the time of RECOVERY during which the immune system is activated and clears out the infection

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28
Q

what is acute convalescence?

A

-The innate and adaptive immune systems clear out the pathogen
-Memory cells make you immune to a subsequent infection

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29
Q

are microbes completely cleared out during an acute infection?

A

yes they are - it is a short term illness because the pathogen is eliminated by the host defenses, the person is usually immune to reinfection

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30
Q

how long is the incubation period for covid?

A

2-14 days

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31
Q

when does the infectious period start in covid?

A

2 days before you start showing symptoms and lasts like 10 days after symptoms show

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32
Q

how long is isolation for with covid?

A

at least 10 days

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33
Q

what is chronic pathogenesis? and examples

A

long-term illness that persists over a long time period.
examples are Hep B, Hep C, HIV, and tuberculosis.

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34
Q

is there an incubation period for chronic?

A

yes

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35
Q

what is the chronic illness?

A

long-lasting

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36
Q

what is the chronic convalescence?

A

-there is no convalescence period so no recovery.
-the pathogen has a way to evade the host’s immune system and persist in hosts body
-may lead to death

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37
Q

do you always have the pathogen in your body during chronic illness?

A

yes, even if it is low #’s

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38
Q

what is latent pathogenesis? and examples

A

illness that can come back at a later stage if the immunity weakens.
Examples are herpes, chickenpox/shingles, and TB

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39
Q

is there an incubation time and illness in latent?

A

yes. both

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40
Q

what is the convalescence in latent?

A

the pathogen does not get completely removed from the host body

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41
Q

in latent, do you have a recovery period? is the pathogen completely removed?

A

you do have a recovery period but the pathogen is NOT completely removed

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42
Q

TB has what type types of pathogenesis?

A

TB is latent and chronic

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43
Q

what is latency in latent pathogenesis?

A

when the pathogen goes into hiding

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44
Q

what is recurrence in latent?

A

when the pathogen comes out of hiding due to the host’s depressed immune system and causes disease. the symptoms the 2nd time around may be the same or different

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45
Q

what are the 4 types of infections? (primary, etc.)

A

primary
secondary
opportunistic
subclinical

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46
Q

what is primary infection?

A

the first infection

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47
Q

what is secondary infection?

A

the second infection that occurs as a result of primary infection

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48
Q

what are examples of secondary infections in children and older people?

A

children: common colds (primary) can lead to ear infections (secondary).
older people: flu (primary) can lead to pneumonia (secondary)

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49
Q

what is opportunistic infection?

A

a disease of opportunity. It occurs when host’s immune system is down like in HIV or cancer patients

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50
Q

what is a subclinical infection?

A

a disease with no noticeable symptoms.

51
Q

what are examples of subclinical infections?

A

-most gonorrhea cases are asymptomatic; if left untreated, damage to reproductive organs can cause infertility in both men and women.
-COVID-19: 40-45% of transmission is due to asymptomatic carriers (that had a subclinical covid-19 case)

52
Q

what are two types of infections (local, etc.)

A

local and systemic

53
Q

what is a localized infection?

A

infection that is limited to a small area

54
Q

what is a systemic infection?

A

a body-wide infection via blood/lymph

55
Q

what are blood-borne systemic infections?

A

they end in -emia
-bacteremia: bacteria in the blood (transient or persistent)
-toxemia: toxins in blood (ex. endotoxin)
-viremia: viruses in blood (eg. flu)
-fungemia: fungi in blood (eg. valley fever)
-parasitemia: parasite in blood (eg. malaria)

56
Q

blood-borne systemic infections can cause what?

A

sepsis or septic shock: generalized inflammatory response to microbes or toxins in the blood

57
Q

a patient with HIV slowly progresses to AIDS when the helper T cell count drops below 200 cells/ul (it is normally ~1000 cells/ul) and the patient develops _______ infections that take advantage when the immune system is down.

A

Opportunistic infections

58
Q

what does “mechanisms of pathogenicity” mean?

A

how do microbes cause an infectious disease?

59
Q

to establish an infection, a pathogen needs to do what 4 things?

A
  1. Adhere to host cells so it is not flushed away (attachment).
  2. Colonize (multiply on surfaces) or invade (penetrate surfaces).
  3. Avoid host defenses to multiply (avoid being killed by immune cells).
  4. Damage the host to facilitate their exit and spread to other hosts.
60
Q

what are virulence factors?

A

factors that allow pathogens to cause disease (make “bad” bugs bad)

61
Q

what happens during step 1 - adhere?

A

Using surface structures to attach to specific receptors on host cells.
-Bacteria: use pili or capsules to attach to receptors on host cells.
-Viruses: use spikes to attach to receptors on host cells

62
Q

what happens during step 2 - colonize or invade?

A
  1. Colonize surfaces:
    -Some pathogens stay at surfaces and do not invade deeper tissues.
    -Ex: C. diff attaches to surfaces of intestinal cells, stays there, multiplies, and forms colonies
  2. Invade deeper tissues:
    -Breach external barriers:
    a. Skin via cuts or wounds
    b. Mucous membranes via uptake methods, ex: Salmonella causes intestinal cells to make membrane ruffles, which engulf the cells.
  3. Spread in tissues or enter the bloodstream.
63
Q

what are two ways that a pathogen does during step 3 - avoid host defenses?

A

Avoid phagocytosis
and
Avoid antibodies

64
Q

what are 3 ways that a pathogen avoids phagocytosis?

A

-Capsules: prevent uptake by phagocytes.
-Phagocyte destruction: by secretion of toxins.
-Survive within phagocyte:
a. Survives through mycolic acids: Mycobacterium tuberculosis with mycolic acids and waxy cell walls prevent their digestion within phagolysosomes.

65
Q

what are three ways that S. pyogenes (that causes strep throat) do to avoid phagocytosis?

A
  1. C5a peptidase: breaks down chemoattractant C5a
  2. Streptolysin O toxin: kills phagocytes.
  3. M protein: inactivates C3b, which helps in opsonization
66
Q

what are C5a and C3b?

A

complement proteins

67
Q

how do pathogens avoid antibodies in step 3 - avoid host defenses?

A

They hide in host cells.
Ex: HIV: induces fusion of infected cell with neighboring target cells; allows it to spread without exiting host cells.
HIV does lyse the cell - it just causes an internal tunnel by fusion the infected cell with all the neighboring cells.

68
Q

why does HIV induce fusion when avoiding antibodies?

A

Because antibodies are located in body fluids extracellular - so in order for HIV not to be killed, they travel intracellularly instead.

69
Q

when pathogens avoid antibodies, what is antigenic variation?

A

When the pathogens change the Ag that the Ab is against, so they keep switching to avoid antibodies.
Examples are:
-Neisseria gonorrhoeae
-Trypanosoma

70
Q

when pathogens avoid antibodies, how do they mimic host antigens?

A

The pathogens are coated with Ags that mimic host Ags. So they get coated so we don’t destroy the “self” cells.
An example is Trypanosoma

71
Q

when pathogens avoid antibodies, how do they perform antibody destruction?

A

When the pathogen makes enzymes that destroy antibodies.
Example: N. gonorrhoeae makes IgA protease

72
Q

what happens in step 4 of pathogens wanting to establish an infection - damage host cells?

A

-Physical lysis of host cell, and is especially seen in viruses (by viruses, killer T cells, and NK cells).
-Induction of immune responses toward self (eg. rheumatic fever, glomerulonephritis).
-Intoxication: most common mechanism of pathogenicity in bacteria by secreting toxins

73
Q

what is the most common mechanism of pathogenicity in bacteria?

A

intoxication

74
Q

what is an endotoxin?

A

-It is part of the cell.
-Lipid A in the outer membrane of Gram-negative bacteria.
-If it is released locally, the host’s immune system will clear it.
-If it is released systemically, this leads to septic shock.

75
Q

what in an exotoxin?

A

-Proteins secreted by bacteria cells in both Gram-negative and Gram-positive bacteria.
-It is then secreted (“exo”) outside.
-Exotoxin secreted into host body or secreted onto and ingested with food.
-It is very potent (small amounts can damage host cells)

76
Q

what type of macromolecule are endotoxins vs. exotoxins?

A

Endotoxins: lipid
Exotoxins: proteins

77
Q

what are local effects of exotoxins?

A

-Local effects can be Staph food poisoning.
This happens by:
-S. aureus secretes toxins on food
-Upon ingestion, the toxin causes nausea, vomiting, stomach cramps, and diarrhea.
-Within a day, the toxin is flushed out, and you feel okay.

78
Q

will antibiotics work as a treatment for staph food poisoning - local exotoxins effects?

A

No, unless S. aureus cells enter and colonize.

79
Q

what is a systemic effect of exotoxins?

A

A systemic effect of exotoxins is Toxic Shock Syndrome (TSS):
-S. aureus and S. pyogenes can invade deep tissues via skin injuries, surgical sites, and mucous membrane abrasions, and then can get into the blood.
-Toxins in the blood lead to systemic inflammation - hypotension (low BP), tachycardia, tachypnea (rapid breathing), and organ failure.

80
Q

can exotoxins damage before activation of immune response?

A

yes

81
Q

how can you be protected from exotoxins?

A

Vaccination with toxoids (active immunity):
tetanus and diphtheria

82
Q

can you administer antitoxins post-exposure (passive immunity) for exotoxins?

A

yes

83
Q

what is botulism etiology? what is botulism?

A

Clostridium botulinum (endospores) - it is an exotoxin

84
Q

what are the characteristics of Clostridium botulinum?

A

Gram-positive
Rod-shaped
Endospore-forming
Obligate anaerobe
Soil dwelling bacterium

85
Q

what is wound botulism?

A

infection of deep penetrating wound with spores

86
Q

what is foodborne botulism?

A

ingestion of toxin in canned food

87
Q

what is infant botulism?

A

spores get into intestines

88
Q

what is latrogenic in botulism?

A

too much toxin injected during cosmetic treatments

89
Q

what is adult botulism?

A

spores get into intestines, which is really rare

90
Q

what does the botulinum exotoxin do?

A

Blocks the release of acetylcholine from the neuron at the neuromuscular junction which prevents muscle contraction and causes flaccid paralysis

91
Q

when can botulinum exotoxin cause death?

A

yes if the diaphragm is paralyzed

92
Q

what does botox stand for?

A

Botulism toxin

93
Q

what are treatments for Botulism?

A

-Open, clean up, and air out the wound (airing it out will kill clostridium because it is an obligate anaerobe).
-Pump the stomach to get rid of toxins.
-Antibiotics and antitoxins
-Supportive care - respirator, feeding tube, etc.
-Neuromuscular junctions take weeks/months to regenerate.

94
Q

why should you not give honey to infants?

A

because there may be spores in botulism within honey

95
Q

what is tetanus etiology? what is tetanus?

A

Clostridium tetani - it is an exotoxin

96
Q

what are tetanus characteristics?

A

Gram-positive
Rod-shaped
Endospore-forming
Anaerobic
Soil-dwelling bacterium

97
Q

how does tetanus cause an infection?

A

Infection of deep penetrating wound with spores, which germinate and produce a toxin

98
Q

what is the main difference between Botulism and Tetanus?

A

Botulism: muscle not contracting
Tetanus: muscle is constantly contracting

99
Q

what does tetanospasmin exotoxin do?

A

Blocks the release of glycine from inhibitory neurons causing the release of acetylcholine at the neuromuscular junction, which leads to the contraction of muscles - and causes rigid paralysis.

100
Q

what can tetanus cause?

A

lock jaw

101
Q

can tetanospasmin exotoxin cause death?

A

can cause death is the diaphragm gets paralyzed

102
Q

what is the treatment of tetanus?

A

-Open, clean up, and air out the wound.
-Antibiotics and antitoxins
-Muscle relaxants, respiratory, feeding tube
-Recovery may take weeks/months

103
Q

what is the prevention of tetanus?

A

Vaccine

104
Q

which type of virulence factor does Clostridium tetani utilize to establish an infection?
1. Capsule
2. Antigenic variation
3. Exotoxin
4. Endotoxin

A
  1. Exotoxin
105
Q

The cause of a disease is known as its:
1. Pathogenicity
2. Etiology
3. Virulence
4. Pathogenesis
5. Epidemiology

A
  1. Etiology
106
Q

Which of the following is incorrectly matched?
1. Acute infection: short-lasting illness.
2. Chronic infection: a disease that lasts a long time.
3. Subclinical infection: infection with no noticeable symptoms.
4. Opportunistic infection: a carrier state.
5. Latent infection: a disease that goes into hiding but can cause periodic outbreaks.

A
  1. Opportunistic infection: a carrier state
107
Q

A body-wide inflammatory response to blood-borne microorganisms and their toxins is called:
1. Bacteremia
2. Toxemia
3. Sepsis
4. Secondary infection
5. Viremia

A
  1. Sepsis
108
Q

The first step in the establishment of infection is:
1. Adherence to host cells
2. Evasion of phagocytosis
3. Invasion of host tissues
4. Spread in the bloodstream
5. Toxin production

A
  1. Adherence to host cells
109
Q

Botulism:
1. Is caused by Clostridium tetani
2. Causes flaccid paralysis
3. Releases an endotoxin
4. Causes a life-threatening kidney failure
5. Is caused by tetanospasmin

A
  1. Causes flaccid paralysis
110
Q

On January 10, a patient received an antibiotic after routine removal of her wisdom teeth. However, after a few days, she was not doing well. She was unable to eat due to severe pain and tightness of the jaw. Four days later, she was admitted to the hospital with severe facial spasms. She reported that on January 7, she had stepped on a sharp object, causing a puncture wound. She cleaned the wound but did not seek medical attention. Was her condition most likely due to an infection or an intoxication (a toxin)? Discuss the etiology and pathogenesis of this condition. Can she transmit this condition to another person? What should her treatment consist of? Is there a way to prevent this condition?

A

Answer: The patient has tetanus (also known as “lockjaw” because initial effects are felt in the jaw muscles). This is an intoxication. It is caused by an exotoxin called tetanospasmin secreted by Clostridium tetani (the patient got the Clostridium bacteria via the puncture wound). The tetanospasmin binds to glycine receptors on inhibitory neurons, so acetylcholine is constantly released to muscle cells, causing rigid paralysis of muscles. This condition is not transmissible. The patient will need intensive therapy including cleansing and debriding of the wound as well as administration of a tetanus antitoxin, muscle relaxants, antibiotics, and supportive care (feeding tube? respirator?). Short of avoiding stepping on the sharp object, the patient could have prevented this condition by getting a tetanus toxoid vaccination (with boosters every 10 years). This prepares the immune system to act before the exotoxin takes hold.

111
Q

The suffix -emia means in the

A

blood

112
Q

Which of the following would be considered a sign of a disease?
1. intense nausea
2. fever of 103 F
3. severe headache
4. throbbing pain
5. all of the these are signs

A
  1. fever of 103 F
113
Q

The chemical nature of endotoxins is that of a:
1. nucleic acid
2. carbohydrate
3. lipid
4. protein

A
  1. lipid
114
Q

The period of time between exposure to an agent and the onset of disease signs and symptoms is called the

A

incubation period

115
Q

What is the difference between a primary pathogen and an opportunistic pathogen?

A

A primary pathogen is a microbe that is able to cause disease in an otherwise healthy individual, while an opportunistic pathogen is a microbe that causes disease only when introduced into an unusual location or into an immunocompromised host.

116
Q

what is an example of a disease that colonizes surfaces only?

A

C. diff - it attaches to surfaces of intestinal cells and stays there, multiplying and forming colonies

117
Q

what is an example of a disease that invades deeper tissues?

A

Salmonella - it causes intestinal cells to make membrane ruffles, which engulf the cells

118
Q

how do mycobacterium tuberculosis avoid phagocytosis?

A

they avoid phagocytosis by surviving within a phagocyte.
they do this because they have waxy cell walls with mycelia acids that prevent their digestion within phagolysosomes.

119
Q

what are two ways in which Trypnosoma avoids antibodies?

A

by antigenic variation and mimicking host antigens

120
Q

what are two ways in which Neiserria gonorrhoease avoid antibodies?

A

by antigenic variation and antibody destruction

121
Q

define flaccid paralysis

A

when there is no muscle contraction due to Botulism

122
Q

define rigid paralysis

A

when there is a constant contraction of muscles due to Tetanus

123
Q

what is the exotoxin called that is secreted by Clostridium tetani?

A

tetanospasmin

Microbiology (53 decks)

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