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Microbiology > Chapters 22 And 23 For Final > Flashcards

Chapters 22 And 23 For Final Flashcards

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Biology 101 flashcards
1
Q

What is the word for a parasite growing and multiplying within or on a host that may or may not result in overt infectious disease?

A

Infection

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2
Q

What is a pathogen?

A

Any parasitic organism that causes infectious disease

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3
Q

What is a primary (frank) pathogen?

A

Causes disease by direct interaction with healthy host

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4
Q

What is an opportunistic pathogen?

A

May be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocompromised

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5
Q

What is Pathogenicity?

A

The ability of a parasite to cause disease

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6
Q

Who was Robert Koch?

A

The father of immunology that identified the causative agent of anthrax

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7
Q

What are Koch’s Postulates?

A
  1. The microorganism must be found in abundance in diseased individuals
  2. The microorganisms must be isolated from the diseased individual and grown in pure culture
  3. The cultured microorganisms must causes disease when re-introduced into a healthy organism (animal model)
  4. The microorganism must be re-isolated from that animal model
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8
Q

An infection with viruses, bacteria, fungi, or Protozoa is called what?

A

An infectious disease

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9
Q

What are signs (aka “read outs” of a patient)?

A

Objective changes in body that can be directly observed

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10
Q

What is the definition of symptoms?

A

Subjective changes experienced by patient

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11
Q

Disease syndrome definition

A

Set of characteristic signs and symptoms

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12
Q

Incubation period definition

A

Period after pathogen entry but before signs and symptoms appear

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13
Q

What is the prodromal stage?

A
  • the onset of signs and symptoms
  • not clear enough for diagnosis
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14
Q

What is the period of illness?

A

Disease is most severe and has characteristic signs and symptoms

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15
Q

What type of immunity is activated during the “period of illness”?

A

Adaptive immunity

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16
Q

What is convalescence?

A

When signs and symptoms begin to disappear

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17
Q

After which event does convalescence appear?

A

After class switching from IgM to IgG

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18
Q

What are the direct modes of spread of communicable infectious disease?

A
  • Horizontal contact (kissing, sex)
  • airborne droplets
  • Vertical contact (mother to child)
  • Vector ( flies and mosquitos)
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19
Q

What are examples of indirect (vehicles) of communicable infectious disease?

A
  • contact fomites (solid surfaces)
  • food, water, biological products (ex: Typhoid Mary)
  • Airborne
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20
Q

What is the stain and shape of Neisseria gonorrhoeae?

A

Gram-negative diplococcus

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21
Q

What type of disease is N. gonorroeae?

A

An STD

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22
Q

Where does N. gonorhoeae colonize most commonly in males vs females?

A

Males: colonizes the urethra
Females: colonizes the cervix

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23
Q

Why is N. gonorrhoea called a superbug?

A

It is called “super” because of its resistance to azithromycin

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24
Q

What is a third generation cephalosporin that can be still be used to treat N. gonorrhoeae despite it being a superbug?

A

Ceftriaxone

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25
Q

What is the difference between Genetic Variation and Gene Regulation?

A

Genetic Variation -> Random switching -> Heterogeneous Population

Genetic Regulation -> Environmental stimulus -> Homogeneous population

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26
Q

In Pilin phase variation, which genes does the promotor control: PilE, pilS1, pilS2, or pil3?

A

PilE

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27
Q

What do pilS1, pilS2, and pilS3 have the tendency to do? What does this lead to?

A

They have the genetic tendency to recombine. This leads to mixed genes and Variability

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28
Q

By varying the pilin amino acid sequence, some N. gonorrhoeae can _______ the adaptive immune response.

A

Escape

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29
Q

What used to be used to treat gonorrhea that can no longer be used due to resistance?

A
  • Penicillin (targets cell wal)
  • Tetracyclines (targets ribosomes)
  • Fluoroquinolones
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30
Q

What is the now recommended treatment for gonorrhea?

A

Ceftriaxone

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31
Q

What is the stain and shape of Staphylococcus aureus?

A

Gram-positive cocci

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32
Q

Where is staphylococcus aureus a huge threat since it is a major nosocomial pathogen?

A

Hospitals

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33
Q

What is the percentage of commensalism/Nasal carraiage of S. aureus?

A

20% stably colonized
60% intermittent carriers

(If you are in this 20% don’t handle for for others)

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34
Q

What type of pathogen is S. aureus?

A

An opportunistic pathogen

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35
Q

What are the features of S. aureus toxins?

A
  • Apoptotic induction/Nutrient acquisition
  • Resistance to oxidative burst killing
  • Binding to host tissues
  • Superantigens
  • Cloaking of opsonins
  • Host cell lysis
  • Impairment of phagocyte recruitment
  • Biofilm
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36
Q

Apoptotic induction/nutrient acquisition:
What three types of enzymes can cause cell degradation via apoptosis?

A

protease, nuclease, and lipase

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37
Q

resistance to oxidative burst killing: ______ catalase is resistant to hydrogen peroxide in the phagosome and has burst protection.

A

SodA

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38
Q

What does binding to host tissues in S. aureus?

A

MSCRAMMs are surface proteins for binding

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39
Q

What do Superantigens do in S. aureus?

A

They can make the immune system go crazy. an example is TSST-1

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40
Q

What is an IgG binding protein that can bind to flip antibody to the outside?

A

Protein A~

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41
Q

What accomplishes the cloaking of opsonins in S. aureus?

A

Capsules

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42
Q

What are capable of Host cell lysis for S. aureus? What symdrome toxin occurs as a result?

A
  • alpha-toxin
  • delta-toxin
  • beta-toxin

scalded skin syndrome toxin

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43
Q

Impairment of phagocyte recruitment: impairs the recruitment of antibodies through ____, ____, and ____.

A

CHIPS, Sak, and Efb

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44
Q

What does biofilm allow?

A

It allows it to be resistant to antibiotics (like a little shield of protection)

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45
Q

Expression of S aureus hemolysis is controlled by what?

A

Cell density

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46
Q

What are the two components of the Two Component System?

A

Histidine Kinase + Response Regulator

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47
Q

What is Quorum sensing?

A

A mechanism where a bacterial population can determine the abundance of itself and others in an environment

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48
Q

Where was Quroum sensing originally discovered?

A

Vibrio fischeri

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49
Q

What does vibrio fischeri make to sense the levels of itself?

A

Autoinducing Peptide (AIP)

High AIP -> makes luciferase

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50
Q

how does Quorum sensing work?

A

When sufficient cells accumulate in an environment, they trigger gene expression and transmission of AIPs

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51
Q

What attaches to the cell wall and uses another “zip code” termed a “sorting signal” and attaches many virulence determinants to the cell wall?

A

Sortase

52
Q

Sortase is a membrane protein conserved in Gram- __________ bacteria?

A

Positive

53
Q

Methicillin resistance is mediated by what?

A

mecA

54
Q

MecA has a _____ affinity for methicillin

A

Low

55
Q

What is the stain and shape of vibrio cholerae?

A

Gram-negative Vibrio

56
Q

what condition is cholera thought to cause the mutation for?

A

Cystic Fibrosis

57
Q

Because cholera is thought to be the reason for the mutation that causes CF, what do CF patients have increased resistance to?

A

Cholera

58
Q

What are Cholera toxins encoded by?

A

A phage

59
Q

What are the symptoms of infection of the small intestine with Vibrio cholera?

A
  • rice water stool
  • severe diarrhea
60
Q

What are the two subunits of the Cholera toxin? how many molecules do each have?

A
  • Subunit A: 2 molecules
  • Subunit B: 5 molecules
61
Q

When the cholera toxin mechanism is in action, does the production of cAMP increase or decrease significantly?

A

Increase

62
Q

During cholera toxin mechanisms of action, the increase of cAMP leads to protein kinase A phosphorylating the CFTR channel. What is the next step in this pathway?

A

Chloride is secreted into the lumen of the gut

63
Q

What do the following characteristics describe?
- expressed in a host
- Pili self-aggregate
- receptor for CTX Phage

A

Toxin-corregulated pilus (TCP)

64
Q

What
- forms microcolonies of V. cholerae
- concentrates toxin to a particular location

A

Pili self-aggregate

65
Q

What are the treatments for cholera?

A

Oral/IV rehydration salts

66
Q

What disease do these characteristics describe?
- Acid-fast gram-positive
- Obligate aerobe
- Discovered by Robert Koch

A

Mycobacterium tuberculosis

67
Q

What does M. tuberculosis have instead of an outer membrane?

A

An outer layer of mycolic acids

68
Q

How do Mycolic Acids differ from from phospholipids?

A
  • normal phospholipids has 13-18 carbons
    - This has. Variable region
  • phospholipids have phosphate region
69
Q

how does M. tuberculosis differ from other gram-positives?

A

It has a layer with Mycolic acids that makes it waxy

70
Q

What virulence factors does M. tuberculosis secrete?

A
  • KatG ( catalase-peroxidase) and SodA (superoxide dismutase)
  • Esat6/CF-10
71
Q

What dos the virulence factor Esat6/CF-10?

A
  • Co-transcribed and form a tight 1:1 complex
  • immunodominant antigen
72
Q

What is Granuloma?

A

Strategy a host uses to wall-off a foreign substance that it cannot eliminate

73
Q

Tuberculosis can remain a persistent cell for years which means what?

A

Once you are infected, you become a carrier for life

74
Q

What is the treatment for the TB Latent Infection?

A

Isoniazid (9 months)

75
Q

When does isoniazid become activated?

A

It can only become activated in the presence of KatG because the active drug form inhibits the synthesis of Mycolic acid

76
Q

What are these treatments for?
- Isoniazid
- Rifampin
- Ethambutol
- Pyrazinamide

A

TB Active Infection

77
Q

What is Malaria caused by?

A

Four species of Plasmodium

78
Q

How is malaria transmitted?

A

By the bite of a female mosquito

79
Q

What is the life cycle of plasmodia protists?

A
  • sporozoite injected with mosquito bite
  • replicates as merozoite in hepatic cells
  • released, enters erythrocytes and replicates
  • lyses erythrocytes- correlated with fever
80
Q

What happens when the schizont breaks?

A

It releases merozoites and infect the liver cells

81
Q

Where do sporozites relicate?

A

Schizont

82
Q

What are the clinical manifestations of malaria?

A
  • chills and fever
  • anemia
  • hypertrophy of the spleen and liver
  • can cause cerebral malaria in children and non immune individuals
83
Q

How is Malaria diagnosed?

A

Uses the Wright or Giemsa-stained red blood cells and serological tests to see the demonstration of parasites

84
Q

treatment, prevention, and control of Malaria

A
  • antimalarial drugs
  • prevention by use of bed netting and insecticides to control mosquitos
  • new vaccine shows promise
85
Q

Why might malaria vaccines not always work?

A

Depending on the stage of the disease, the surface proteins completely change and therefore changes the antigens. Vaccines are surface protein specific, so if the vaccine is distributed at the wrong stage in the cycle, it might be ineffective

86
Q

What percent of 5-7 month olds who received the malaria vaccine were Protected?

A

40%

87
Q

The _____ vaccine trains the immune system to attack the malaria parasite, which is spread by mosquito bites.

A

RTS,S

88
Q

What is sickle-cell disease?

A

An endemic in Africa that is a human evaluation to fight Malaria

89
Q

What is thought to be the most pressure on human evolution in recent history?

A

Sickle-cell disease

90
Q

What are the causes of Sickle-cell disease?

A
  • Abnormal hemoglobin
  • under low oxygen, hemoglobin forms polymers and the red blood cell elongates
91
Q

RBCs are normally elastic. What disease prevents elasticity?

A

sickle-cell disease

92
Q

Why is sickle-cell bad for malaria?

A
  • the cels aren’t elastic anymore
  • cells lose before the parasite can replicate to high numbers
93
Q

In sickle-cell, are patients immune to malaria?

A

NO, they are resistant and NOT immune

94
Q

What are treatments for malaria?

A
  • Quinine
  • Chloroquine
  • Atovaquone/progunil
95
Q

What does Atovaquone/proguanil do?

A

It inhibits plasmodium’s electron transport chain/ DHFR

96
Q

What is Leishmaniasis caused by and how is it spread?

A

It is caused by different Leishmania species and it is spread from host-to-host through a sand fly vector

97
Q

What are the two forms of Leishmaniasis?

A
  • Cutaneous
  • Visceral
98
Q

What are the two forms of the Leishmaniasis parasite?

A
  • Promastigote
  • Amastigote
99
Q

The Promastigote form of Leishmaniasis in (people/the fly)

A

In the fly

100
Q

What is the difference in morphology between Promastigote and amstigote?

A

Promastigote is oblong and flagellated in the fly while the Amastigote is oval and has a rudimentary flagella in people

101
Q

Where are the lesions of cutaneous leishmaniasis? what do they cause?

A

The mouth, nose, throat, and skin

they cause disfigurement and excessive scarring

102
Q

True or False: people who have cutaneous leishmaniasis have permanent immunity after healing

A

True

103
Q

Can cutaneous leishmaniasis heal without treatment?

A

Yes it can, but it can take weeks, months, or years and typically leaves a scar

104
Q

What system does viscera Leishmaniasis (Kala-azar) involve?

A

The monocyte-macrophage system

105
Q

What are the clinical manifestations of visceral Leishmaniasis?

A
  • intermittent fever and enlargement of spleen and liver
  • may be fatal
106
Q

True or False: people that recover from Visceral Leishmaniasis get permanent immunity

A

True

107
Q

What is the mortality rate of untreated Visceral leishmaniasis?

A

Nearly 100%

108
Q

What is the treatment, prevention, and control for Leishmaniasis?

A
  • anti parasite therapy
  • vector and reservoir control
  • epidemiological surveillance
109
Q

What is the bacteria that causes Chagas’ disease? What is the vector?

A

Trypanosoma cruzi

“Kissing” bugs or “assassin” bugs

110
Q

what regions is Chagas’ disease present in?

A

Tropical Latin American regions

111
Q

What is acute Chagas’ disease?

A

Rapid onset, trypanosome moves through the bloodstream, enters cells and becomes Amastigote, replicates

112
Q

At which stage of Chagas’ might treatment be effective?

A

The Acute stage

113
Q

What are the symptoms of Chagas’ disease?

A
  • May have no/mild symptoms (swelling/reddening of the bite site)
  • further symptoms develop
    • eye swelling
    • lymph node infections
    • fever
    • malaise
    • spleen/liver may enlarge
114
Q

What happens in chronic Chagas’ disease?

A
  • Amastigotes reach the heart, GI and other cells
  • replicate causing heart disease and other disorders due to the destruction of parasitized cells in the liver, spleen, lymph nodes, GI, and central nervous system
115
Q

Are there treatment options available at the chronic stage of Chagas’ disease? Why or why not?

A

No. Vaccines are not effective due to the antigenic variation of the trypanosome

116
Q

How does chronic Chagas’ disease emerge?

A
  • heart disease
    • often leads to sudden death
  • bowel abnormalities
    • can lead to malnutrition
117
Q

What are the two treatment drugs for Chagas’ disease?

A
  • Benznidazole
  • Nifurtimox
118
Q

What bacteria causes African sleeping sickness? What is the vector?

A

Trypanosoma brucei

Tsetse fly vector

119
Q

What are the two types of African sleeping sickness?

A

East African and West African

120
Q

What causes East African sleeping sickness?

A

T. brucei rhodesiense

121
Q

What causes West African sleeping sickness?

A

T. brucei gambiense

122
Q

What are the symptoms of African sleeping sickness when it spreads through the blood?

A

Fever, headache, sweating, and swelling of the lymph nodes

123
Q

What are the symptoms of African sleeping sickness when it spreads through the CNS?

A

Behavioral changes, drowsiness during the day (insomnia at night), coma

124
Q

What are the treatment options for African sleeping sickness?

A
  • Suramin (for 6 weeks)
  • Melarsoprol (very toxic and can be fatal due to arsenic compound)
  • Pentamidine
125
Q

what is a side effect of treatment of Melarsoprol for African sleeping sickness?

A

Arsenic poisoning

Microbiology (11 decks)

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