Midterm 1 (Lectures 1-6) Flashcards

1
Q

What is microbiology the study of?

A

The study of microorganisms that are too small to be seen by the naked eye (need microscope to view).

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2
Q

Who invented the (simple, light) microscope? What did they examine? What did they call microorganisms at the time?

A

Antoni van Leeuwenhoek
- Examined water
- “Animalcules” = microorganisms (saw tiny animals, fungi, algae, unicellular protozoa)

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3
Q

What are the 6 categories of Leeuwenhoek’s microorganisms? Describe if they are prokaryotic or eukaryotic.

A
  1. Bacteria => prokaryotic
  2. Archaea => prokaryotic
  3. Fungi => eukaryotic
  4. Protozoa => eukaryotic
  5. Algae => eukaryotic
  6. Small multicellular animals => eukaryotic
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4
Q

Prokaryotes lack a…?

A

Nucleus

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5
Q

Leeuwenhoek microorganisms can be seen with a _____ microscope.

A

Light microscope

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6
Q

What category of microbes are NOT included in Leeuwenhoek’s microorganisms? What microscope is used to view them?

A
  • Viruses
  • Electron microscope
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7
Q

What are acellular agents that can cause disease?

A

Viruses

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8
Q

Why are viruses considered acellular/noncellular?

A
  • Lack complex cellular structures
  • Cannot carry out any metabolic pathway
  • Can neither grow or response to the environment
  • Cannot reproduce independently
  • Need the chemical and structural components of the cell they infect to replicate
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9
Q

What is the “Golden Age of Microbiology?”

A
  • 1800’s
  • Improved microscopes
  • New lab techniques
    = Microbiology at forefront of scientific disciplines
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10
Q

What 4 questions lead to major discoveries during the golden age of microbiology?

A
  1. Is spontaneous generation of microbial life possible?
  2. What causes fermentation?
  3. What causes disease?
  4. How can we prevent infection and disease?
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11
Q

What is abiogenesis?

A

Aristotle’s theory that “living things arise from nonliving matter.”

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12
Q

Describe Francesco Redi’s experiments.

A

Decaying meat:
1) Flask unsealed = maggots
- Meat exposed to flies = laid eggs = maggots

2) Flask sealed = no maggots
- Meat was kept isolated from flies, maggots
never developed

3) Flask covered with gauze = maggots

  • Maggots didn’t arise from the meat itself but from fly eggs
  • Scientists began to doubt Aristotle’s theory of abiogenesis
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13
Q

Scientists agreed that large animals could not arise spontaneously, but believed ________ could.

A

Microbes

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14
Q

How did John L. Needham’s experiments reinforce the idea of abiogenesis?

A
  • Boiled (to kill the microorganisms) beef gravy and infusions of plant material in vials
  • Tightly sealed vials with cork
  • Some days later, microorganisms were detected in the infusions
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15
Q

How did Lazzaro Spallanzani disprove Needham’s findings? What were his conclusions?

A
  • Boiled infusions for 1 hour
  • Sealed the vials airtight
  • Infusions remained clear unless he broke the seal

Conclusions:
- Needham failed to heat vials sufficiently or had not sealed them tightly enough
- Microbes exist in air and can contaminate experiments
- Spontaneous generation of microbes does NOT occur; all living things arise from other living things

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16
Q

Why did critics still not believe Spallanzani’s findings?

A
  • Thought sealed vials did not allow enough air for organisms to survive, and
  • Prolonged heating destroyed the “life force”
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17
Q

How do “swan-necked” flasks work in creating a sterile environment?

A
  • Allow air flow
  • Dust particles or microbes stay in the tube part (“the bend of the neck”), not allowed into flask
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18
Q

How did Louis Pasteur further prove abiogenesis is not possible?

A
  • Experiments with swan-necked flasks
  • Upright flasks = no microbial growth even after 18 months
  • Tilted flask (“break the seal”) = dust from the bend seeped back into flask = cloudy infusion with microbes within a day
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19
Q

Who discovered the cause of fermentation?

A

Louis Pasteur

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20
Q

What was a problem in 19th century France?

A

Spoiled wine (was sour, acidic)
- Wine makers funded research to find cause (of fermentation and spoilage)

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21
Q

What were the differing opinions of scientists for the cause of fermentation?

A
  • Some believed it was air
  • Some believed it was living organisms
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22
Q

Describe Louis Pasteur’s experiments that showed the causes of wine spoilage and fermentation.

A

Flasks of grape juice, heated:
1) Flask sealed
- No fermentation, no microbes = abiogenesis NOT possible

2) Swan-necked flasks (open to air via curved neck)
- No fermentation, no microbes = air does NOT ferment grape juice

3) Flask inoculated with bacteria and sealed
- Bacteria reproduce; acids are produced = bacteria cause wine spoilage

4) Flask inoculated with yeast and sealed
- Yeasts reproduce; alcohol is produced = yeast causes fermentation (converts sugars to alcohol)

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23
Q

What did Pasteur’s experiments lead to?

A
  • Development of pasteurization
  • Began the field of industrial microbiology (intentional use of microbes for manufacturing products like bread, cheese, etc.)
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24
Q

What is pasteurization?

A
  • Process of heating liquids just enough to kill most bacteria
  • Increases shelf-life of product
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25
Q

What did Eduard Buchner’s experiments demonstrate?

A
  • Demonstrated that fermentation does not require living cells
  • Showed enzymes promote chemical reactions (i.e. the microbe’s enzymes cause fermentation)
    => This work began the field of biochemistry
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26
Q

Who HYPOTHESIZED that microorganisms are responsible for causing diseases?

A

Louis Pasteur
- “Germ Theory of Disease”

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27
Q

What are pathogens?

A

Organisms that cause disease in a host.

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28
Q

Who was the first to SHOW that bacteria can cause disease? Explain.

A

Robert Koch (studied etiology)
- Animals suffering from anthrax => found rod-shaped bacteria (Bacillus anthracis) that produce endospores in blood
- Injected endospore in mice => produced anthrax

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29
Q

What is etiology?

A

The study of causative agents of disease.

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30
Q

Describe Koch’s 4 postulates.

A
  1. Causative agent must be found in every case of disease and be absent from healthy hosts
  2. Agent must be isolated and grown outside the host
  3. When agent is introduced to healthy susceptible host, the host must get the disease
  4. Same agent must be found in the diseased experimental host
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31
Q

Describe some advances in laboratory microbiology that Robert Koch and his colleagues are known for.

A
  • Simple staining techniques
  • First photomicrograph of bacteria
  • First photograph of bacteria in diseased tissue
  • Techniques for estimating bacterial number in a solution
  • Autoclaving (use of steam to sterilize growth media)
  • Use of Petri dishes
  • Bacterial transfer techniques
  • Bacteria as distinct species
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32
Q

What is autoclaving?

A

Use of steam to sterilize growth media.

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33
Q

Who recommended hand-washing for medical students?

A

Ignaz Semmelweis
- Observed women giving birth where medical students were trained dying from puerperal fever (Streptococcus infection)
- Medical students recommended to wash hands with chlorinated lime water

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34
Q

Who invented antiseptic techniques?

A

Joseph Lister
- Sprayed wounds, surgical incisions, and dressings with carbolic acid (phenol)

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35
Q

Who founded the first school for nurses?

A

Florence Nightingale (Nightingale School for Nurses)
- Introduced cleanliness and other antiseptic techniques into nursing practice

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36
Q

What is epidemiology?

A

The study of the spread, frequency, and distribution of diseases.
- When and where?
- How are they transmitted?

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37
Q

John Snow laid the foundation for epidemiology through his work with __________ cases.

A

Cholera
- London epidemic in 1854
- Mapped occurrence of cholera cases => showed that they centered around a public water supply (water contaminated with sewage)
- Infection control (set standard for good public hygiene to prevent spread of diseases)

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38
Q

Who set the standard for good public hygiene to prevent spread of diseases?

A

John Snow

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39
Q

Who coined the term “vaccination” or “vaccine?”

A

Edward Jenner (field of immunology)
- Named after Vaccinia virus

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40
Q

Edward Jenner found that inoculation of a boy with pus collected from a milkmaid’s _______ lesion (mild disease) made the boy immune to the deadly ________ infection.

A

1) cowpox 2) smallpox
- Intentionally infected the boy (introduced antigens to boost/prime immune system)

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41
Q

Who discovered an arsenic-based chemical drug that was active against the causative agent of syphilis (Treponema pallidum)?

A

Paul Ehrlich (field of chemotherapy)
- “Magic bullets”
- Serious side effects in humans (arsenic = toxic)

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42
Q

What is chemotherapy?

A

Development and use of drugs to treat infectious diseases.

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43
Q

What 2 questions does the “Modern Age of Microbiology” focus on?

A
  1. What are the basic chemical reactions of life? (biochemistry and microbial metabolism)
    - Design of herbicides and pesticides
    - Disease diagnosis and patients’ responses to treatment
    - Treatment of metabolic diseases
    - Drug design
  2. How do genes work?
    - Microbial genetics
    - Molecular biology
    - Recombinant DNA technology
    - Gene therapy
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44
Q

What are the most diverse group of cellular microbes?

A

Prokaryotes
- Thrive in various habitats
- Exist in a variety of shapes (rods, spirals, etc.)

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45
Q

What is the typical size of prokaryotic cells?

A

1.0 µm in diameter or smaller.

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46
Q

Name 2 characteristics of prokaryotic cells.

A
  • Lack a nucleus
  • Lack membrane-bound internal structures
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47
Q

Which 2 domains are prokaryotic organisms divided into?

A
  1. Bacteria
  2. Archaea
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48
Q

In prokaryotes, transcription (mRNA synthesis) and translation (protein synthesis) occur _____________.

A

Simultaneously

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49
Q

What are some functions of bacterial cell walls?

A
  • Provide structure, shape, and protection from osmotic forces
  • Assist in cell attachment
  • Can provide antimicrobial drug resistance
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50
Q

What bacteria lack cell walls?

A

Mycoplasma

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51
Q

What bacteria are considered the smallest free-living cells?

A

Mycoplasma
- Often mistaken for viruses due to small size and lack of cell wall
- Have most other features of prokaryotic cells

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52
Q

What is the primary component of bacterial cell walls?

A

Peptidoglycan

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53
Q

What is the structure of peptidoglycan?

A
  • Polysaccharide made up of 2 different sugars (NAG & NAM)
  • Peptide chains cross-link the sugar chains (tetrapeptide crossbridge)
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54
Q

How do Gram-positive and Gram-negative bacteria differ in their cell walls?

A
  • Gram-positive bacteria have a thick peptidoglycan layer that contains unique chemicals (teichoic/lipoteichoic acids)
  • Gram-negative bacteria have a thin peptidoglycan layer and an outer membrane containing phospholipids, proteins, and lipopolysaccharides (LPS)
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55
Q

How do Gram-positive and Gram-negative stain? Why?

A
  • Gram-positive = purple (retain colour even after washing with alcohol due to thicker layer of peptidoglycan)
  • Gram-negative = pink (lose purple dye after washing with alcohol, counterstain with pink dye)
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56
Q

What is Lipid A in Gram-negative bacteria, and why is it significant?

A
  • Lipid A is part of the LPS outer membrane
  • Endotoxin that can cause fever, vasodilation, inflammation, shock, and blood clotting
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57
Q

What is the prokaryotic cytoplasmic (plasma) membrane referred to as? What is it composed of?

A

Phospholipid bilayer
- Lipids
- Integral proteins (embedded in lipid bilayer)
- Peripheral proteins (outside, attached to lipid bilayer)

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58
Q

What are glycocalyces, and what are the 2 types?

A
  • Glyocalyces = gelatinous, sticky substance (polysaccharides, polypeptides, or both) that surrounds the outside of prokaryotic cells

1) Capsule = firmly attached to cell surface
- Composed of organized repeating units of organic chemicals
- Provides protection and aids in attachment

2) Slime Layer = loosely attached
- Sticky, water-soluble layer
- Aids in attachment

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59
Q

What structure is responsible for movement of prokaryotic cells? Describe its function.

A

Flagella (structure varies depending on if Gram-positive or Gram-negative)
- Rotation propels bacterium through environment
- Rotation is reversible (counterclockwise or clockwise)
- Bacteria moves in response to stimuli (taxis) => attracted to source of stimuli (e.g., food) or repelled from toxin

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60
Q

What are the 3 main parts of bacterial flagella? Describe them.

A
  1. Filament => outside the cell
  2. Hook => attaches filament to basal body
  3. Basal body => anchors flagella (filament + hook) to cell wall
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61
Q

Name different types of flagella arrangements.

A

Arrangements are suited to bacterial environment:
- Peritrichous (multiple flagella spread out all over bacterial cell)
- Single polar (single flagellum found at one end of cell)
- Tuft of polar (tuft of flagella extending from one end or both ends of cell)

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62
Q

What family of bacteria have a unique flagellar structure and thus motion? Explain.

A

Spirochetes = Gram-negative spiral-shaped bacteria
- Endoflagella form an axial filament
- Corkscrew motion

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63
Q

Spirochetes include bacteria that cause what diseases? Name the bacteria.

A
  • Lyme disease => Borrelia burgdorferi
  • Syphilis => Treponema pallidum
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64
Q

What are fimbriae?

A

External structure of prokaryotic cells:
- Sticky, bristle-like projections (shorter than flagella)
- Aid in bacterial adherence
- Help form biofilms

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65
Q

What are biofilms? What external structure serves an important function in biofilms?

A
  • Biofilm = thin gelatinous layer (colony) of bacterial cells
  • Fimbriae serve important function
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66
Q

What are (conjugation) pili?

A
  • Special type of fimbriae (longer than fimbriae, but shorter than flagella)
  • Form conjugation channels (connections between bacteria) => transfer DNA from one cell to another during conjugation
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67
Q

How many pili do bacteria typically have?

A

1-2 per cell

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68
Q

Rank flagella, fimbriae, and pili from largest to smallest.

A

Flagella > pili > fimbriae

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69
Q

What is the cytosol in prokaryotic cells? What does it contain?

A
  • Liquid portion of cytoplasm
  • Contains cell’s DNA in region called the nucleoid
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70
Q

What is the nucleoid in prokaryotic cells? Where is it found?

A
  • Nucleoid = region containing the prokaryotic cell’s DNA
  • Found in the cytosol
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71
Q

Name structures found in the cytoplasm of prokaryotic cells.

A
  • Inclusions / Inclusion Bodies (may include reserve deposits of chemicals)
  • Ribosomes (polypeptides, rRNA)
  • Cytoskeleton (protein fibers like actins, tubulins)
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72
Q

What are some roles of the cytoskeleton in the cell?

A
  • Cell division
  • Cell shape
  • Segregate DNA molecules
  • Move through the environment
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73
Q

What are endospores, and which bacteria form them?

A

Defensive structures formed (inside the cell) under unfavourable conditions by some Gram-positive bacteria, such as Bacillus and Clostridium.

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74
Q

How do some bacteria form endospores?

A
  1. DNA is replicated (new copy of DNA)
  2. Instead of going through mitosis, invaginate to synthesize membrane around new DNA (forespore)
  3. Cytoplasmic membrane grows and engulfs forespore within a second membrane
  4. Vegetative cell’s DNA disintegrates
  5. Cortex of peptidoglycan is deposited between the 2 endospore membranes, and chemicals accumulate within endospore
  6. A spore coat forms around the endospore (protects from harsh conditions)
  7. Endospore matures and is released from original cell
  8. Under favourable conditions, each endospore germinates to form a
    vegetative cell
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75
Q

Why are endospores significant to healthcare and food safety?

A
  • Resistant to extreme conditions like heat, radiation, and chemicals
  • Don’t divide/grow (challenge for treating diseases)
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76
Q

How many membranes does an endospore have? In addition, what other structure does it have that aids in its protection?

A

2 membranes and a spore coat.

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77
Q

Name some shapes prokaryotic cells can take.

A
  • Coccus
  • Coccobacillus
  • Bacillus (rod-shaped)
  • Vibrio (“V” shape)
  • Spirillum
  • Spirochete
  • Pleomorphic (many different structures)
  • Star
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78
Q

What are the 3 main methods of asexual reproduction in prokaryotic cells? Briefly describe them.

A
  1. Binary fission => cell replicating DNA and splits into 2 daughter cells
  2. Snapping division => part of vegetative cell breaks off and becomes new bacterial cell
  3. Budding => new genetic material forms cytoplasm + membrane, outgrows from parent cell
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79
Q

What is the most common method of reproduction in prokaryotes?

A

Binary fission

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80
Q

What unique reproduction method is found in Epulopiscium?

A

Viviparity – live offspring emerge from the body of the dead mother cell (first noted case of viviparous behaviour in prokaryotic world).

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81
Q

What is the largest known bacteria, that is also NOT pathogenic.

A

Epulopiscium

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82
Q

Arrangements of prokaryotic cells are a result of…?

A
  • Planes of cell division
  • Separation of daughter cells
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83
Q

Modern prokaryotic classification is based on genetic relatedness of _____ sequences.

A

rRNA (conserved, don’t change)

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84
Q

What domain of prokaryotes are NOT known to cause disease?

A

Archaea

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85
Q

Describe some characteristics of archaea.

A
  • Lack true peptidoglycan
  • Cell membrane lipids have branched hydrocarbon chains
  • Reproduce by binary fission, budding, or fragmentation
  • Are cocci, bacilli, spirals, or pleomorphic
  • Include extremophiles (thermophiles, acidophiles, halophiles)
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86
Q

What is the largest group of archaea?

A

Methanogens => convert CO2, H2, and organic acids to methane gas (CH4)

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87
Q

What are deeply branching bacteria, and where are they found?

A
  • Autotrophic (synthesize their own nutrients) bacteria similar to the earliest bacteria
  • Live in habitats similar to those that existed on early Earth
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88
Q

Give 2 examples of deeply branching bacteria.

A
  • Aquifex
  • Deinococcus
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89
Q

What bacteria is considered to represent earliest branch of bacteria?

A

Aquifex

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90
Q

What bacteria has an outer membrane similar to Gram-negatives, BUT stains Gram-positive?

A

Deinococcus

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91
Q

What do phototrophic bacteria contain?

A

Photosynthetic lamellae that contain different pigments.

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92
Q

What are the 5 groups of phototrophic bacteria? What are the divisions based on?

A

Divided based on pigments and source of electron for photosynthesis (most are autotrophic):
1. Cyanobacteria (blue-green bacteria)
2. Green sulfur bacteria
3. Green non-sulfur bacteria
4. Purple sulfur bacteria
5. Purple non-sulfur bacteria

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93
Q

What are low G+C Gram-positive bacteria?

A

Gram-positive bacteria with less than 50% G+C content in their genome.

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94
Q

What phylum are low G+C Gram-positive bacteria classified in? What groups are included?

A

Firmicutes phylum
- 3 groups:
1. Clostridia
2. Mycoplasmas
3. Other low G+C Gram-positive bacilli and cocci

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95
Q

Name some low G+C Gram-positive bacteria.

A
  • Clostridium tetani
  • Clostridium perfringens
  • Clostridium difficile
  • Mycoplasma
  • Bacillus anthracis
  • Bacillus thuringiensis
  • Bacillus polymyxa
  • Bacillus lichenifomis
  • Listeria (monocytogenes)
  • Lactobacillus
  • Streptococcus
  • Enterococcus
  • Staphylococcus (aureus)
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96
Q

Describe characteristics of Clostridia low G+C Gram-positive bacteria.

A
  • Rod-shaped
  • Obligate anaerobes
  • Many form endospores
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97
Q

Which bacteria is associated with tetanus?

A

Clostridium tetani

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98
Q

Which bacteria is associated with gas gangrene?

A

Clostridium perfringens
(causes gas to form in soft tissues, leads to amputation)

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99
Q

Clostridium difficile is associated with _________.

A

Diarrhea
(C. difficile thrives when gut microbiome is disrupted)

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100
Q

What microbes are related to Clostridium?

A
  • Epulopiscium
  • Sulfate-reducing microbes
  • Selenomonas (live as part of biofilm/plaque that forms on teeth)
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101
Q

What is the appearance of Mycoplasma colonies described as?

A

“Fried egg”

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102
Q

What diseases do some species of Mycoplasma cause?

A
  • Pneumonia
  • Urinary tract infections
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103
Q

Describe some characteristics of Mycoplasma low G+C Gram-positive bacteria.

A
  • Facultative or obligate anaerobes
  • Lack cell walls
  • Smallest free-living cells
  • Colonize mucous membranes of the respiratory and urinary tracts
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104
Q

What do Mycoplasma colonize?

A

Mucous membranes of the respiratory and urinary tracts.

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105
Q

Describe characteristics of Bacillus low G+C Gram-positive bacteria.

A
  • Many are common in soil
  • Form endospores
  • Some members cause human and animal disease
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106
Q

What bacteria causes anthrax (inhalation and cutaneous types)?

A

Bacillus anthracis

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107
Q

What bacteria is used by farmers and gardeners as an insecticide (its toxin is)?

A

Bacillus thuringiensis

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108
Q

Bacitracin antibiotic is produced by what bacteria?

A

Bacillus lichenifomis

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109
Q

Bacillus polymyxa produces what antibiotic?

A

Polymyxin

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110
Q

Describe some characteristics of Listeria (monocytogenes) low G+C Gram-positive bacteria.

A
  • Rod-shaped
  • Contaminates milk and meat products
  • Capable of reproducing under refrigeration
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111
Q

What conditions are caused by Listeria monocytogenes?

A
  • Can cross placenta in pregnant women and infect the fetus
  • Meningitis and bacteremia in immunocompromised individuals
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112
Q

Describe some characteristics of Lactobacillus low G+C Gram-positive bacteria.

A
  • Grows in the body, but rarely causes disease
  • Used in the production of various foods (yogurt, buttermilk, pickles, etc.)
  • Used as a probiotic
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113
Q

What diseases do Streptococcus and Enterococcus cause?

A
  • Pharyngitis
  • Scarlet fever
  • Impetigo
  • Fetal meningitis
  • Pneumonia
  • Wound infections
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114
Q

There are various strains of multi-drug-resistant _____________.

A

Streptococci

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115
Q

What bacteria is one of the most common inhabitants of humans?

A

Staphylococcus
- Produces toxins and enzymes that contribute to disease

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116
Q

What diseases does Staphylococcus aureus cause?

A

Invades the body and causes diseases such as:
- Bacteremia
- Food poisoning
- Toxic shock syndrome
- Pneumonia
- Wound infections

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117
Q

_________________ is resistant to antimicrobial drugs (penicillin and cephalosporin).

A

Methicillin-resistant Staphylococcus aureus (MRSA)

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118
Q

Name some high G+C Gram-positive bacteria.

A
  • Corynebacterium (diphtheriae)
  • Mycobacterium tuberculosis
  • Mycobacterium leprae
  • Actinomycetes (Actinomyces, Nocardia, Streptomyces)
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119
Q

Describe Corynebacterium high G+C Gram-positive bacteria. Name one that causes a disease.

A
  • Pleomorphic aerobes and facultative anaerobes
  • Corynebacterium diphtheriae causes diphtheria
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120
Q

Describe characteristics of Mycobacterium high G+C Gram-positive bacteria.

A
  • Aerobic rods that sometimes form filaments
  • Slow-growing (often require months to show a visible colony on agar growth medium)
  • Cell wall contains mycolic acid (long carbon-chain)
  • Acid-fast bacilli (AFB) => stain with acid-fast stains such as the Ziehl-Neelsen stain
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121
Q

What bacteria causes tuberculosis?

A

Mycobacterium tuberculosis

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122
Q

What bacteria causes Hansen’s disease (leprosy)?

A

Mycobacterium leprae

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123
Q

Describe Actinomycetes high G+C Gram-positive bacteria, naming the important genera.

A

Form branching filaments resembling fungi:
- Actinomyces => some species are opportunistic pathogens
- Nocardia
- Streptomyces

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124
Q

What high G+C Gram-positive bacteria can degrade many pollutants?

A
  • Nocardia (can degrade waxes, petroleum, hydrocarbons, detergents, etc.)
  • Part of Actinomycetes
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125
Q

______________ species produce important antibiotics (chloramphenicol, erythromycin, tetracycline).

A

Streptomyces

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126
Q

What is the largest and most diverse group of bacteria?

A

Gram-negative proteobacteria

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127
Q

Name the 6 classes of Gram-negative proteobacteria.

A
  1. Alphaproteobacteria
  2. Betaproteobacteria
  3. Gammaproteobacteria
  4. Deltaproteobacteria
  5. Epsilonproteobacteria
  6. Zetaproteobacteria
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128
Q

Name some alphaproteobacteria.

A
  • Rickettsia
  • Brucella
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129
Q

Describe characteristics of Rickettsia Gram-negative bacteria.

A
  • Alphaproteobacteria
  • Aerobic rods that live and reproduce inside mammalian cells (intracellular pathogen)
  • Transmitted through bite of an arthropod (vectors of disease)
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130
Q

What human diseases do Rickettsia alphaproteobacteria cause?

A
  • Typhus
  • Rocky Mountain spotted fever
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131
Q

What is an obligate intracellular pathogen? Give examples.

A
  • Pathogen that has to infect a host organism’s cells in order to reproduce and survive
  • Examples: Viruses, Rickettsia alphaproteobacteria
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132
Q

Describe Brucella alphaproteobacteria and diseases it causes.

A
  • Can survive phagocytosis by WBCs
  • Causes brucellosis in humans (characterized by chills, sweating, fatigue, and fever)
  • In animals it causes spontaneous abortions and sterility
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133
Q

What bacteria causes brucellosis in humans? What are the symptoms?

A
  • Brucella
  • Symptoms: chills, sweating, fatigue, and fever
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134
Q

Name some betaproteobacteria.

A
  • Neisseria (gonorrhoeae) => diplococci that inhabit mucous membranes
  • Bordetella (pertussis)
  • Burkholderia
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135
Q

What bacteria causes gonorrhea?

A

Neisseria gonorrhoeae

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136
Q

What bacteria causes whooping cough (pertussis)?

A

Bordetella pertussis

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137
Q

What bacteria colonizes moist environmental surfaces, and thus is found in respiratory passages of cystic fibrosis patients?

A

Burkholderia
- Respiratory tract produces extra fluid/mucus in CF patients (genetic mutation) = creates ideal conditions for bacteria to grow/infect

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138
Q

What is the largest and most diverse class of proteobacteria? Name its 5 subgroups.

A

Gammaproteobacteria:
1. Intracellular pathogens => thrive inside phagolysosomes in WBCs (acidic pH)
2. Glycolytic facultative anaerobes
3. Pseudomonads
4. Purple sulfur bacteria
5. Methane oxidizers

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139
Q

Name some
intracellular pathogenic gammaproteobacteria.

A
  • Legionella
  • Coxiella
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140
Q

Name the 3 families of glycolytic facultative anaerobes (gammaproteobacteria), and the bacteria they include.

A
  1. Enterobacteriaceae (Escherichia, Salmonella, Proteus, Shigella, Yersinia, Klebsiella)
  2. Vibrionaceae (Vibrio)
  3. Pasteurellaceae (Haemophilus)
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141
Q

What bacteria causes Legionnaires’ disease?

A

Legionella (intracellular pathogenic gammaproteobacteria)

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142
Q

What bacteria causes Q fever?

A

Coxiella (intracellular pathogenic gammaproteobacteria)

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143
Q

What do Escherichia gammaproteobacteria cause?

A

Gastroenteritis

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144
Q

What do Salmonella gammaproteobacteria cause?

A

Typhoid (Salmonella typhi)

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145
Q

What do Proteus gammaproteobacteria cause?

A

UTI (urinary tract infection)

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146
Q

What do Shigella gammaproteobacteria cause?

A

Shigellosis

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147
Q

What do Yersinia gammaproteobacteria cause?

A

Plague (Yersinia pestis)

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148
Q

What do Klebsiella gammaproteobacteria cause?

A

Pneumonia

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149
Q

What do Vibrio gammaproteobacteria cause?

A

Cholera (Vibrio cholerae)

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150
Q

What do Haemophilus gammaproteobacteria cause?

A
  • Meningitis
  • Middle ear infections
  • Pneumonia
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151
Q

What do Pseudomonads (gammaproteobacteria) cause?

A

Urinary tract, ear, lung, infections (important pathogens of humans and animals)
- Often in burn patients

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152
Q

What is the significance of Pseudomonads in healthcare?

A

They often cause infections in burn patients (because their skin is compromised).

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153
Q

Name some deltaproteobacteria (wide variety of metabolic types).

A
  • Desulfovibrio
  • Bdellovibrio
  • Myxobacteria
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154
Q

Describe Bdellovibrio bacteria.

A
  • Gram-negative deltaproteobacteria
  • Single flagella
  • Pathogen of other Gram-negative bacteria
  • Lives in periplasmic space (b/n cytoplasm and cell wall) => induces death
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155
Q

Describe epilsonproteobacteria. Give examples of some.

A

Gram-negative rods, vibrios, or spirals:
- Campylobacter jejuni
- Helicobacter pylori

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156
Q

What bacteria causes gastroenteritis?

A

Camplyobacter jejuni (epilsonproteobacteria)

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157
Q

What bacteria causes peptic ulcer disease?

A

Helicobacter pylori (epilsonproteobacteria)

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158
Q

Describe zetaproteobacteria.

A
  • First discovered based on DNA sequences (DNA is common in oceans)
  • Only 2 organisms have been cultured
  • Mariprofundus ferroxydans is the only species to be formally named
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159
Q

Only 2 organisms have been cultured of ___________________.

A

Zetaproteobacteria

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160
Q

________________ is the only species to be formally named of zetaproteobacteria.

A

Mariprofundus ferroxydans

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161
Q

Name other Gram-negative bacteria aside from the proteobacteria.

A
  • Chlamydias
  • Spirochetes (Treponema pallidum, Borrelia burgdorferi)
  • Bacteroides
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162
Q

What Gram-negative bacteria causes syphilis?

A

Treponema pallidum

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163
Q

What Gram-negative bacteria causes Lyme disease?

A

Borrelia burgdorferi

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164
Q

Describe Chlamydia bacteria.

A
  • Gram-negative
  • Grow intracellularly in mammals, birds, and some invertebrates
  • Some are smaller than viruses (0.2 µm in diameter)
  • Most common sexually transmitted bacteria in the US
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165
Q

What is the most common sexually transmitted bacteria in the US?

A

Chlamydia bacteria

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166
Q

Describe Bacteroides and the diseases/symptoms they can cause.

A
  • Gram-negative bacteria
  • Inhabit skin & digestive tracts of humans and animals
  • Non-pathogenic normally, but opportunistic (become pathogenic if person becomes immunocompromised)
  • Some species cause infections => diarrhea, fever, foul-smelling lesions, gas, and pain
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167
Q

Describe characteristics of eukaryotic cells.

A
  • Have nucleus
  • Have internal membrane-bound organelles
  • 10-100µm in diameter
  • May have cell wall (e.g., plants), cilium, or flagella (structurally different from prokaryotes)
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168
Q

What eukaryotes have a cell wall?

A
  • Fungi
  • Algae
  • Plants
  • Some protozoa
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169
Q

Plant cell walls are made of…?

A

Cellulose

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170
Q

Fungal cell walls are composed of…?

A
  • Cellulose
  • Chitin (most abundant polymer in nature)
  • and/or Glucomannan
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171
Q

Algal cell walls are composed of a variety of _______________.

A

Polysaccharides

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172
Q

All eukaryotic cells have _____________________.

A

Cytoplasmic membranes

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173
Q

Describe eukaryotic cytoplasmic membranes.

A
  • Fluid mosaic of phospholipids + proteins
  • Steroid lipids help maintain fluidity
  • Contain membrane rafts = regions of lipids & proteins
  • Selectively permeable (control movement into and out of cell)
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174
Q

Describe eukaryotic flagella.

A
  • Shaft composed of tubulin => arranged to form MTs within cell membrane
  • Filaments anchored to cell by basal body
  • Single or multiple; generally found at one pole of cell
  • Undulate rhythmically to propel the cell in their environment (DON’T ROTATE)
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175
Q

Describe the structure (MT arrangement) of eukaryotic flagella.

A
  • Cell membrane extends over entire length
  • 9+2 MT arrangement (9 doublets outside, 2 central)
  • Basal body has 9+0 MT arrangement (9 triplets)
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176
Q

Describe reproduction in eukaryotic cells.

A
  • Requires division of nucleus and cytoplasm
  • Sexual (gametes + zygotes formed) or asexual (cell dividing into 2 daughter cells)
  • Algae, fungi, and some protozoa reproduce both sexually and asexually
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177
Q

What are the 2 types of nuclear division in eukaryotes?

A

Nucleus contains genetic material (has to be replicated to create copy of genome):
1. Mitosis => partitions replicated DNA equally between 2 nuclei
2. Meiosis => partitions chromatids into 4 nuclei (gametes)

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178
Q

Describe cytokinesis in eukaryotes.

A

Cytokinesis = cytoplasmic division:
- Different types (formation of a cell plate, formation of a partition furrow, or budding)
- In some algae and fungi, postponed or does not occur at all, resulting in multinucleated cells called coenocytes

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179
Q

What are the different types of cytokinesis in eukaryotes?

A
  1. Formation of a cell plate
  2. Formation of a partition/cleavage furrow
  3. Budding => yeast (fungi)
    - Bud grows inside, separates from parent to become daughter cell
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180
Q

What does postponed or skipped cytokinesis result in? What eukaryotes does this happen in?

A
  • Result in multinucleated cells called coenocytes
  • In some algae and fungi
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181
Q

How were eukaryotic organisms classified? How are they classified now?

A
  • Early: grouped organisms based on structural similarities
  • Modern: based on similarities in nucleotide sequences (genetic relatedness)
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182
Q

What are the 5 eukaryotic microorganisms?

A
  1. Protozoa
  2. Fungi
  3. Algae
  4. Slime molds
  5. Water molds

=> Include both human pathogens and organisms vital for human life

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183
Q

Describe characteristics of protozoa.

A
  • Unicellular eukaryotic cells
  • Lack cell wall
  • Motile (cilia, flagella, and/or pseudopods)
  • Great morphological diversity
  • Different stages in life cycle (trophozoite, cyst)
  • Require moist environments
  • Most are chemoheterotrophic
  • Very few are pathogens
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184
Q

Protozoa are ______________trophic, meaning…?

A
  • Chemoheterotrophic
  • Obtain nutrients by phagocytizing bacteria, decaying organic matter, other protozoa, or the host tissues
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185
Q

What are 2 life stages of a protozoa?

A
  1. Trophozoite => motile feeding stage
  2. Cyst => resting stage (more resistant to harsh conditions)
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186
Q

Name some pathogenic protozoa.

A

Mostly infect immunocompromised individuals (e.g., people infected with HIV):
- Trichomonas => STDs
- Giardia => GI infection
- Trypanosoma => sleeping sickness
- Leishmania => cutaneous leishmaniasis
- Plasmodium => malaria
- Cryptosporidium => GI infection
- Toxoplasma => toxaplasmosis
- Entamoeba => GI infection

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187
Q

What type of microbe is Trichomonas? What diseases does it cause?

A
  • Protozoa
  • Sexually transmitted diseases (STDs)
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188
Q

What protozoa cause gastrointestinal infection?

A
  • Giardia
  • Cryptosporidium
  • Entamoeba
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189
Q

What microbe causes toxoplasmosis?

A

Toxoplasma (protozoa)

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190
Q

What microbe causes malaria?

A

Plasmodium (protozoa)

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191
Q

What microbe causes sleeping sickness?

A

Trypanosoma (protozoa)

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192
Q

Leishmania, a _____________, causes ________________.

A
  • Protozoa
  • Cutaneous leishmaniasis
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193
Q

Describe characteristics of fungi.

A
  • Chemoheterotrophic
  • Cell walls typically composed of chitin
  • Include yeasts (unicellular), molds, mushrooms
  • Some fungi are dimorphic => produce both yeast-like and mold-like shapes in response to environmental conditions
194
Q

Some fungi are dimorphic, meaning…?

A

Produce both yeast-like and mold-like shapes in response to environmental conditions.

195
Q

What are the 2 basic morphologies of fungi? Describe them.

A
  1. Molds => composed of long filaments called hyphae
    - Septate hyphae = multiple cells separated by walls/septa
    - Aseptate hyphae = one large cell containing multiple nuclei
  2. Yeasts => small, globular, and composed of a single cell
196
Q

Describe reproduction in fungi; are they asexual or sexual?

A
  • All have some means of asexual reproduction (involve mitosis + cytokinesis)
  • Most also reproduce sexually (form gametes => have 1/2 the genetic material from parent and fuse to form diploid organism)
197
Q

What is the significance of fungi?

A
  • Decompose dead organisms and recycle their nutrients
  • Help plants absorb water and minerals
  • Used in manufacture of foods/beverages
  • Produce antibiotics (e.g., penicillin) and other drugs
  • Serve as important research tools (e.g., yeast in genetics)
  • Can spoil fruit, pickles, jams, and jellies
  • 30% cause diseases of plants, animals, and humans
198
Q

___% of fungi cause diseases of plants, animals, and humans.

199
Q

__________ are diseases caused by fungi.

200
Q

What is dermatophytosis?

A

Infection of the skin by fungi (e.g., Athlete’s foot, ringworm).

201
Q

What fungi cause dermatophytosis?

A
  • Trichophyton
  • Microsporum
  • Epidermophyton floccosum
202
Q

__________ causes infection of the mucous membranes? What disease does it cause specifically?

A
  • Candida albicans (opportunistic pathogen)
  • Candidiasis, yeast infections
203
Q

What fungi cause respiratory tract infections? What diseases do they specifically cause?

A
  • Coccidioides => coccidioidomycosis
  • Blastomyces dermatitidis => blastomycosis
  • Histoplasma capsulatum => histoplasmosis
  • Pneumocytis jirovecii => pneumonia
204
Q

What microbe causes histoplasmosis?

A

Histoplasma capsulatum (fungi)

205
Q

What fungi causes pneumonia?

A

Pneumocytis jirovecii

206
Q

Describe characteristics of algae.

A
  • Photoautotrophs
  • Non-pathogenic
  • Differ widely in distribution, morphology, reproduction, and biochemical traits
  • Most are aquatic (live in the photic zone of fresh, brackish, and salt bodies of water)
207
Q

What are the different morphologies of algae?

A
  • Unicellular
  • Colonial
  • Simple multicellular bodies
208
Q

Describe reproduction in unicellular and multicellular algae.

A

Unicellular:
- Asexually (mitosis + cytokinesis)
- Sexually (gametes form zygotes that undergo meiosis)

Multicellular:
- Asexually (fragmentation => part of the body/organ can break away)
- Sexually with alternation of generations

209
Q

What are helminths? Why are they of microbiological interest?

A
  • Helminths = parasitic worms
  • Have infective microscopic/diagnostic stages (e.g., eggs/larvae) that occur in samples of blood, urine, and feces
210
Q

What are vectors? What are the 2 types?

A

Vectors = animals that carry pathogens:
1. Mechanical vectors => carry pathogen without being infected (physical transport/transmission)
2. Biological vectors => infected, pathogen completes part of their life cycle

211
Q

What 2 classes of arthropods are disease vectors? Describe them and give examples.

A
  1. Arachnida
    - Archanids have 4 pairs of legs
    - Ticks, some mites
  2. Insecta
    - Adult insects have 3 pairs of legs and 3 body regions
    - Fleas, lice, flies, and mosquitoes
212
Q

What are the most important arthropod vectors vectors of disease?

A

Mosquitoes (carry viruses and protozoan diseases like malaria)

213
Q

Describe characteristics of viruses.

A
  • Minuscule (need electron microscope to view)
  • Acellular
  • Exist in extracellular and intracellular states
  • Contain either DNA or RNA (never both)
  • Cause infections in humans, animals, plants, and bacteria
  • Do not carry out metabolic pathways
  • Do not reproduce independently
  • Use the host cell’s metabolic pathways for replication
214
Q

Why are viruses considered obligate intracellular pathogens/parasites?

A

To survive, need to infect host cell and use its machinery to replicate and produce new virus progeny.

215
Q

Describe the extracellular and intracellular states of viruses.

A
  • Extracellular: virions (don’t grow/reproduce) composed of capsid, nucleocapsid, envelope, and nucleic acid
  • Intracellular: viral nucleic acid (capsid falls apart)
216
Q

What are the components of a virion?

A
  • Capsid
  • Nucleic acid (DNA or RNA)
  • Envelope (in some cases)
217
Q

What are viruses without an envelope called?

A

Naked viruses

218
Q

What is one of the largest viruses?

A

Smallpox virus (even larger than some bacteria, like Chlamydia)

219
Q

Describe the viral genome.

A
  • DNA or RNA (never both)
  • Single-stranded (ss) or double-stranded (ds)
  • ssRNA viruses can be (+) or (-)
  • Can be linear and segmented, or single and circular
  • Genomes are much smaller than those of cells (depend on host cell for most of their metabolic processes => only need genes for capsid proteins, enzymes, etc.)
220
Q

Viruses are classified based on their…?

A

Genome (DNA viruses or RNA viruses)

221
Q

What virus infects the tobacco plant?

A

Tobacco mosaic virus

222
Q

Most viruses infect only a particular host’s cells: what determines what host a virus infects?

A
  • Affinity of viral surface proteins for complementary proteins on host cell surfaces
  • Some viruses can only infect a particular kind of cell in a host (e.g., neurotropic virus only infects neurons)
  • Some viruses can infect many kinds of cells or many different hosts
223
Q

What is the structure/function of a viral capsid?

A
  • Houses and protects viral nucleic acid
  • Helps determine the shape of the virion
  • Composed of protein subunits called capsomeres (made of single or multiple protein types)
  • Facilitates attachment and entry in non-enveloped viruses
224
Q

What are the 3 basic viral shapes?

A
  1. Helical => “rod structure” (e.g., tobacco mosaic virus)
  2. Polyhedral
  3. Complex => “bullet” (e.g., rabies virus)
225
Q

How do viruses acquire an envelope, and what is its composition?

A
  • Acquired from the host cell membrane during replication or release (e.g., through budding)
  • Composed of phospholipid bilayer and proteins
  • Some proteins are virally coded glycoproteins (spikes)
226
Q

What is the role of the viral envelope?

A

Envelope proteins/glycoproteins help in host recognition, binding, and entry.

227
Q

Are enveloped or naked viruses more fragile?

A

Enveloped viruses (e.g., wash with soap detergent = become vulnerable and lose infectivity)

228
Q

What is virus classification based on?

A
  1. Type of nucleic acid
  2. Presence of an envelope
  3. Shape and size
  • Viral genera have only been organized into families
229
Q

What is the difference between positive-sense and negative-sense RNA viruses?

A
  • +ssRNA = similar to mRNA; can be directly translated into proteins
  • -ssRNA = complementary to mRNA; must be converted to +ssRNA before translation
230
Q

Why are viruses dependent on host cells for replication?

A

They lack organelles and enzymes necessary for independent reproduction.

231
Q

Viral replication usually results in ____________ of host cell.

A

Death & lysis

232
Q

What are the 5 stages of viral replication?

A
  1. Attachment
  2. Entry (capsid disassembles)
  3. Synthesis
  4. Assembly
  5. Release
233
Q

How do animal viruses attach to host cells?

A
  • Via chemical attraction between viral proteins (capsid/spike) and cell receptors = recognition
  • Use glycoprotein spikes or other molecules (co-receptors) for attachment
234
Q

After viral attachment to host cell, what allows for its entry?

A

Change in host cell’s membrane structure upon attachment allows for entry.

235
Q

What are the 3 main entry mechanisms for animal viruses? Describe them.

A
  1. Direct penetration
    - Viral proteins attach to host receptors
    - Viral genome is released from capsid into host cell
  2. Membrane fusion
    - Spikes attach to host receptors
    - Envelope fuses with host cell membrane
    - Virus enters host cell and disassembles its capsid
  3. Endocytosis
    - Spikes attach to host receptors
    - Host cell membrane engulfs virus
    - Virus enters cell in endosome
    - After entry, virus leaves endosome and disassembles its capsid
236
Q

How does viral genome synthesis differ for DNA and RNA viruses?

A
  • DNA viruses => replicate in the nucleus
  • RNA viruses => replicate in the cytoplasm
237
Q

Describe synthesis of dsDNA viruses.

A

Viral genome synthesis:
- Each strand of DNA acts as a template for its complementary DNA strand

Viral protein synthesis:
- mRNA is synthesized by the host RNA polymerase
- Viral proteins are made in the cytoplasm

238
Q

What dsDNA virus is synthesized differently (an exception)?

A

Hepatitis B viruses
- Replicate DNA from an RNA intermediary (DNA => RNA => DNA)
- Reverse transcription

239
Q

What are viruses with ssDNA genomes called?

A

Parvoviruses

240
Q

Describe synthesis of ssDNA viruses.

A
  • DNA strand folds back on itself (regions that have complementary base pairs) to form dsDNA
  • That dsDNA is then replicated by cellular DNA polymerase
  • Newly replicated strand is released as ssDNA
241
Q

What are the 4 types of RNA viruses?

A
  • +ssRNA
  • Retroviruses (+ssRNA)
  • -ssRNA
  • dsRNA
242
Q

Retroviruses are a type of _______ virus.

243
Q

What type of viruses convert their RNA to DNA through reverse transcription?

A

Retroviruses

244
Q

For RNA viruses, replication of RNA genome is often performed by what viral enzymes?

A
  • RNA-dependent RNA polymerase (host cells don’t replicate RNA)
  • Reverse transcriptase / RNA-dependent DNA polymerase (converts RNA => DNA)
245
Q

Describe synthesis of +ssRNA viruses.

A

Viral genome synthesis:
- Transcription of complementary -ssRNA by viral RNA polymerase
- Further transcription: -ssRNA acts as template to create copies of +ssRNA

Viral protein synthesis:
- +ssRNA acts as mRNA => directly translated

246
Q

Describe synthesis of -ssRNA viruses.

A

Viral genome synthesis:
- Transcription of complementary +ssRNA by viral RNA polymerase
- Further transcription: +ssRNA acts as template to create copies of -ssRNA

Viral protein synthesis:
- Transcribed +ssRNA also acts as mRNA => directly translated

247
Q

Describe synthesis of dsRNA viruses.

A

Viral genome synthesis:
- Unwinding of dsRNA into -ssRNA and +ssRNA strands
- Transcription of complementary -ssRNA/+ssRNA strands by viral RNA polymerase
- Newly transcribed strands synthesized into dsRNA

Viral protein synthesis:
- Transcribed +ssRNA also acts as mRNA => directly translated

248
Q

What enzyme do retroviruses use for replication?

A

Reverse transcriptase (RNA-dependent DNA polymerase)

249
Q

What is an example of an retrovirus?

250
Q

Describe retrovirus synthesis.

A

Viral genome synthesis:
- In the cytoplasm, reverse transcriptase converts the viral +ssRNA into viral DNA
- Viral DNA transports into the nucleus and integrates into the host genome
- Host genome is transcribed, creating new viral +ssRNA

Viral protein synthesis:
- The newly transcribed viral +ssRNA acts as mRNA => directly translated

251
Q

Where do DNA and RNA viruses assemble?

A
  • DNA viruses = in the nucleus
  • RNA viruses = in the cytoplasm
252
Q

How do naked vs. enveloped viruses get released from host cells?

A
  • Naked viruses => released by exocytosis or lysis (lysis kills infected cell)
  • Enveloped viruses => released by budding to acquire part of host membrane (does NOT kill the cell)
253
Q

Why do enveloped viruses cause persistent infections?

A

Enveloped viruses are more persistent because they do not kill the host cell upon release (budding).

254
Q

What determines the number of viruses produced in a host cell?

A
  • Type of virus
  • Virus size
  • Initial health of host cell
255
Q

What is viral latency?

A

Period from the time virus infects and till symptoms show.

256
Q

Describe latency of animal viruses.

A
  • When animal viruses remain dormant in host cells (proviruses)
  • May be prolonged for years with no viral activity (e.g., HIV develops into AIDS)
  • Incorporation of provirus into host DNA is permanent
257
Q

What are proviruses or latent viruses?

A
  • Viruses that remain dormant in host cells
  • Viral genome becomes integrated into host DNA (provirus e.g., HIV)
258
Q

How do viruses contribute to cancer (neoplasia, uncontrolled cell division) development?

A
  • Activation of oncogenes (promote cell division)
  • Inactivation of tumour suppressor genes (normally repress cell division)
  • Some viruses carry oncogenes or promote existing ones in hosts
259
Q

______% of human cancers are associated with virus infections.

260
Q

Which human cancers are associated with viruses?

A
  • Burkitt’s lymphoma: Epstein-Barr Virus (EBV)
  • Hodgkin’s disease: Epstein-Barr Virus (EBV)
  • Kaposi’s sarcoma: Kaposi sarcoma-associated herpesvirus
  • Cervical cancer: Human papilloma virus (HPV)
  • Liver cancer: Hepatitis B (causes cirrhosis of liver)
261
Q

What cancers is Epstein-Barr Virus (EBV) associated with?

A
  • Burkitt’s lymphoma
  • Hodgkin’s disease
262
Q

Kaposi’s sarcoma can be caused by what virus?

A

Kaposi sarcoma-associated herpesvirus

263
Q

Cervical cancer can be caused by what virus?

A

Human papilloma virus (HPV)

264
Q

Why can’t viruses be grown in standard microbiological media?

A

Viruses require a host cell to replicate and produce new virions (need cell system).

265
Q

What are the 3 types of media used for culturing animal viruses?

A
  1. Mature organisms (ethical concerns, expensive to maintain)
  2. Embryonated eggs (inexpensive, sterile, nutrient-rich medium)
  3. Cell cultures (continuous, inexpensive and easy to maintain)
266
Q

Why are embryonated eggs (e.g., fertilized chicken eggs) used for culturing animal viruses?

A
  • Embryonic tissues provide ideal site for growing vaccines
  • Inexpensive, sterile, nutrient-rich medium
267
Q

What are viroids? Describe their characteristics.

A
  • Extremely small, circular pieces of ssRNA
  • Lack a capsid
  • Do NOT code for proteins
  • Infectious and pathogenic in plants (adhere to complementary plant RNA => plant enzyme degrades dsRNA, resulting in disease state)
268
Q

How are viroids pathogenic in plants?

A

1) Viroid (ssRNA) adheres to complementary plant RNA
2) Plant enzyme degrades the dsRNA
3) Results in disease state

269
Q

What are prions?

A
  • Proteinaceous infectious agents
  • Do NOT contain nucleic acids (no genome)
  • Cause disease by misfolding normal cellular PrP into prion PrP
270
Q

What is the difference between cellular prions and pathogenic prions?

A

Cellular (c-PrP):
- Has alpha-helices

Pathogenic (p-PrP):
- Has beta-pleated sheets

271
Q

What organisms make cellular prions? What is thought to be their function?

A
  • c-PrP made by all mammals
  • Function not well-understood but thought to be involved in normal synaptic development/function
272
Q

How do pathogenic prions reproduce and cause damage to infected tissues?

A
  • Multiply by conversions => p-PrP causes c-PrP to refold into p-PrP (change in conformation), thus increasing [p-PrP]
  • p-PrP group into multimers => get deposited as amyloid plaque (cause damage)
273
Q

What are diseases caused by prions called? How are they transmitted? Are there any treatments?

A
  • Spongiform encephalopathies (large vacuoles form in brain = “spongy”)
  • Transmitted by ingestion, transplantation, or contact of mucous membranes with infected tissues
  • NO standard treatment for any prion disease
274
Q

What diseases do prions cause in humans and animals?

A

Human prion diseases:
- Variant Creutzfeldt-Jakob disease (vCJD)
- Kuru (fatal neurodegenerative disorder)

Animal prion diseases:
- Mad cow disease (Bovine SE)
- Scrapie (sheep & goats)

275
Q

Why are prion diseases difficult to treat?

A

No standard treatment exists.

276
Q

What are antimicrobial agents? What do they take advantage of?

A
  • Drugs that can treat infectious diseases
  • Take advantages of differences between microbial cells and mammalian cells
  • Target cellular structures and pathways specific to microbial cells to reduce side effects
277
Q

What are the different ways to classify antimicrobial agents?

A
  1. Type of microbe affected (anti-bacterial, anti-fungal, anti-viral, etc.)
  2. Targeted pathways (cell wall inhibitor, RNA transcription inhibitor, protein synthesis inhibitor, etc.)
  3. Spectrum of action (narrow vs. broad spectrum)
  4. Effects (microbiocidal vs. microbiostatic)
278
Q

What is the difference between narrow-spectrum vs. broad-spectrum antimicrobial drugs?

A
  • Narrow = effective against few organisms
  • Broad = effective against many organisms (not the best choice => can also disrupt normal microbiota and cause 2ndary infections)
279
Q

What is the difference between microbiocidal vs. microbiostatic drugs?

A
  • Microbiocidal = kills microbes
  • Microbiostatic = inhibit microbial growth
280
Q

What is one example why an antimicrobial drug may have toxic side effects in mammalian cells?

A

Can affect mitochondria of mammalian cells, as mitochondria are related to bacteria (endosymbiotic theory).

281
Q

Who is credited with the discovery of penicillin? What microbe produces penicillin? Briefly describe its antibiotic effect.

A
  • Alexander Fleming
  • Produced by mold (fungus) Penicillium chrysogenum
  • Inhibitor of cell wall synthesis (peptidoglycan) = β-lactam
282
Q

Who coined the term “chemotherapy” to describe chemicals that selectively killed pathogens?

A

Paul Ehrlich (“magic bullets” = arsenic compounds that killed bacteria that caused syphillis)

283
Q

What term describes chemicals that selectively kill pathogens?

A

Chemotherapy

284
Q

Who discovered sulfanilamide (type of sulfonamide) and why was it significant?

A

Gerhard Domagk; it was the first commercially produced antimicrobial drug for bacterial infections.

285
Q

Who coined the term “antibiotics” to describe antimicrobial agents produced naturally by organisms? Explain.

A
  • Selman Waksman
  • Discovered that other microorganisms are sources of useful antimicrobials (e.g., streptomycin is produced by Streptomyces)
286
Q

What term describes antimicrobial agents produced naturally by organisms?

A

Antibiotics

287
Q

What are the differences between semisynthetic and synthetic antimicrobials?

A
  • Semisynthetic = chemically altered antibiotics for effectiveness (e.g., longer lasting, easier to administer)
  • Synthetic = antimicrobials completely synthesized in a lab
288
Q

What are the 6 mechanisms of action of antimicrobial drugs?

A
  1. Inhibiting cell wall synthesis
  2. Inhibition of protein synthesis
  3. Disruption of cytoplasmic membrane
  4. Inhibition of general metabolic pathway
  5. Inhibition of DNA or RNA synthesis
  6. Inhibition of pathogen’s attachment or entry into host cell
289
Q

Why are new bacterial cell walls synthesized? How?

A

Synthesize new cell wall to grow and divide:
- New “building blocks” (sugar units = NAG + NAM) are synthesized in the cytoplasm,
- Transported across the cell membrane to the cell wall,
- And incorporated into existing cell wall
- Peptide linkages (cross-links) are formed to hold the sugar chains together

290
Q

Describe β-lactam antibiotics and how they work. What is an example of one?

A
  • Functional groups = β-lactam rings
  • Effective against Gram-positive bacteria
  • Inhibit enzymes that cross-link NAM subunits in peptidoglycan = weak cell wall = bursts from osmotic pressures
  • Examples: Penicillin, Methicillin, Imipenem, Cephalothin
291
Q

Why are β-lactams more effective against Gram-positive bacteria?

A
  • Gram-positive bacteria have a thick peptidoglycan layer that β-lactams can easily target
  • Gram-negative bacteria have an outer membrane that prevents easy access to peptidoglycan
292
Q

What are the benefits of semisynthetic derivatives of β-lactams?

A
  • More stable in acidic environments = can be taken orally
  • More readily absorbed
  • Less susceptible to deactivation
  • More active against a broader range of bacteria
293
Q

What are some non-β-lactam drugs that inhibit cell wall synthesis? Describe them.

A
  • Vancomycin & cycloserine => interfere with alanine-alanine bridges that link NAM subunits in many Gram-positive bacteria
  • Bacitracin => blocks NAG & NAM transport from the cytoplasm
  • Isoniazid & ethambutol => disrupt mycolic acid formation in Mycobacterium species (e.g., tuberculosis, leprosy)
294
Q

What antibiotics interfere with alanine-alanine bridges that link NAM subunits in many Gram-positive bacteria?

A
  • Vancomycin
  • Cycloserine
295
Q

What antibiotic blocks NAG & NAM transport from the cytoplasm?

A

Bacitracin

296
Q

What antibiotics disrupt mycolic acid formation in Mycobacterium species?

A
  • Isoniazid
  • Ehtambutol
297
Q

What are the drawbacks of antimicrobial drugs that inhibit peptidoglycan synthesis (β-lactams)?

A
  • Have no effect on existing peptidoglycan layer
  • Only effective for actively growing bacteria
  • Less effective against Gram-negative bacteria
  • Bacteria can develop resistance via β-lactamase enzyme (penicillinase), which breaks the β-lactam ring found in the drugs (now inactive)
298
Q

How are fungal cell walls different from mammalian cells?

A

They are made of various polysaccharides not found in mammalian cells, including β1,3-glucan.

299
Q

How do echinocandins (antifungal drug) work?

A
  • Inhibit β1,3-glucan synthase (enzyme that synthesizes β1,3-glucan), disrupting fungal cell wall formation
  • Results in weaker cell wall, susceptible to osmotic shock
300
Q

What fungal species are echinocandins effective against?

A
  • Fungicidal against Candida spp
  • Fungistatic against Aspergillus spp
301
Q

What antibiotic inhibits β1,3-glucan synthase in fungal cells?

A

Echinocandins

302
Q

How do polyenes disrupt fungal membranes? Give examples of these drugs.

A
  • Bind to ergosterol in fungal cell membranes, forming channels/pores that disrupt membrane integrity
  • Examples: Nystatin, Amphotericin B
303
Q

Why are bacteria not susceptible to polyenes?

A

Lack sterols in membrane.

304
Q

Why do polyenes have some toxicity to humans?

A

Human cholesterol (found in cell membrane) is similar to fungal ergosterol, causing side effects.

305
Q

What antimicrobial drugs inhibit ergosterol synthesis? What microbes do they affect?

A
  • Azoles (e.g., fluconazole)
  • Allylamines (e.g., terbinafine)
  • Are antifungals & antiprotozoans (harmless to humans because cells do not produce ergosterol)
306
Q

Polymyxin is an antibiotic produced by ____________________.

A

Bacillus polymyxa

307
Q

How do polymyxins (antibiotic) work?

A
  • Disrupt cell membrane of Gram-negative bacteria
  • Toxic to human kidneys/liver = reserved for topical use (less toxic when applied to skin)
308
Q

_____________ disrupts transport across cell membrane of Mycobacterium tuberculosis.

A

Pyrazinamide

309
Q

Pyrazinamide (antibiotic) is effective against…?

A

Intracellular, non-replicating bacterial cells.

310
Q

Prokaryotic ribosomes are ___S.

A

70S (30S & 50S)

311
Q

Eukaryotic ribosomes are ___S.

A

80S (40S & 60S)

312
Q

Why can drugs that inhibit protein synthesis (i.e. target prokaryotic ribosomes) have some side effects in mammalian cells?

A

Mitochondria contain 70S ribosomes similar to prokaryotic ribosome.

313
Q

What are some examples of antimicrobial drugs that inhibit protein synthesis?

A
  • Aminoglycosides (streptomycin, gentamicin, tetracyclines)
  • Chloramphenicol
  • Lincosamides
  • Streptogramins
  • Macrolides
  • Fomivirsen
  • Oxazolidinone
  • Mupirocin
314
Q

How do aminoglycosides (e.g., streptomycin, gentamicin) work?

A

Change shape of the 30S small subunit, preventing correct mRNA codon reading (induce kink).

315
Q

How do tetracyclines inhibit protein synthesis?

A

Block tRNA docking site (don’t allow tRNA to bring new AA), terminating protein elongation.

316
Q

What are some side effects of tetracyclines?

A

Discolouration of teeth and nails in some patients.

317
Q

How does chloramphenicol inhibit protein synthesis?

A

Binds to the enzymatic site of 50S large subunit, preventing peptide bond formation.

318
Q

How do lincosamides, streptogramins, & macrolides (e.g., erythromycin) inhibit protein synthesis?

A

Bind to sites on the 50S large subunit; prevent ribosome movement along mRNA from one codon to next (synthesis stops).

319
Q

How does fomivirsen (synthetic anti-viral drug) inhibit protein synthesis?

A
  • Antisense nucleic acid
  • Complementary to specific mRNA of the pathogen, creating dsRNA that blocks ribosome attachment
  • dsRNA eventually degraded
320
Q

____________ stops protein synthesis by blocking initiation of translation.

A

Oxazolidinone (prevents ribosome binding to mRNA)

321
Q

How does Mupirocin inhibit protein synthesis?

A

Interferes with charging of tRNA => selectively inhibits isoleucyl-tRNA synthetase (chain terminates where isoleucine is supposed to be present).

322
Q

_____________ is used as a topical drug to treat skin infection by Gram-positive bacteria.

323
Q

What are the different types of antimetabolic agents?

A
  • Drugs that interfere with the electron transport chain (in protozoa & fungi)
  • Heavy metals (arsenic, mercury, antimony) inactivate enzymes
  • Agents that disrupt tubulin polymerization & glucose uptake (many protozoa & parasitic worms)
  • Drugs that block viral activation (keep virus in dormant stage, prevent triggering pathway)
  • Metabolic antagonists (e.g., sulfa drugs block nucleotide synthesis)
324
Q

How do sulfonamides (sulfa drugs) inhibit nucleotide synthesis?

A

Inhibit nucleotide biosynthetic pathway:
- Are structural paralogs of para-aminobenzoic acid (PABA) = precursor in folic acid synthesis
- Compete with PABA for the enzyme that converts it to dihydrofolic acid (competitive inhibitors)

325
Q

Why do sulfa drugs not affect humans?

A

Humans obtain folic acid from diet and do not rely on the pathway the drugs target.

326
Q

___________ affects the same nucleotide synthesis pathway as sulfonamides.

A

Trimethoprim

327
Q

How do protease inhibitors work against HIV?

A

Prevent HIV proteins from being processed by proteases, stopping assembly of new virions.

328
Q

What antimicrobial drugs inhibit prokaryotic DNA gyrase?

A
  • Quinolones
  • Fluoroquinolones
  • Prevent proper coiling and uncoiling of replicating bacterial DNA
329
Q

How does rifampin inhibit RNA transcription?

A

It binds to bacterial RNA polymerase, inhibiting transcription.

330
Q

____________ binds to bacterial DNA; prevents normal transcription.

A

Clofazimine

331
Q

Rifampin & clofazimine are used for treatment of _________________.

A

Mycobacterium diseases (tuberculosis & leprosy)

332
Q

How do reverse transcriptase inhibitors work?

A
  • Treatment of retroviral infection (e.g., HIV)
  • Block viral replication by inhibiting reverse transcription of viral RNA genome into complementary DNA
333
Q

How do nucleotide or nucleoside analogs inhibit DNA/RNA synthesis? What are they effective against?

A
  • Structually similar to purines/pyrimidines => get incorporated into DNA/RNA, interfering with their function
  • Distort shape of DNA/RNA; prevent further replication, transcription, or translation
  • Most often used against viruses (once virus infects cell, has to replicate = more susceptible to analogs)
  • Also effective against rapidly dividing cancer cells
334
Q

How do attachment antagonists work? Give examples of such drugs.

A

They block interactions between viral attachment proteins and host receptors (required for attachment & entry into cell).
- Examples: pleconaril, arildone

335
Q

Pleoconaril is a synthetic drug antagonist of receptors for…

A

Picornaviruses (cold viruses, poliovirus, coxsackievirus)

336
Q

___________ is a synthetic drug that prevents uncoating of poliovirus.

A

Arildone (interrupts viral replication cycle)

337
Q

What are Pleconaril and Arildone used for?

A

Pleconaril prevents attachment of picornaviruses; Arildone prevents poliovirus uncoating.

338
Q

What are the characteristics of an ideal antimicrobial drug?

A
  • Readily available
  • Inexpensive
  • Chemically stable (at room temp, long shelf-life, maintains concentration in body)
  • Easily administered (e.g., orally)
  • Non-toxic & non-allergenic
  • Selectively toxic against wide range of pathogens (doesn’t harm beneficial microflora)
339
Q

What are clinical considerations in prescribing antimicrobial drugs?

A
  • Spectrum of actions
  • Effectiveness
  • Route of administration
  • Safety and side effects
340
Q

Why are broad-spectrum antibiotics not always desirable?

A

Can kill normal microflora and reduce microbial antagonism, resulting in:
- Secondary infections => opportunisitic pathogens become pathogenic because they lose competition from normal microflora (e.g., Candida yeast)
- Superinfections => one or more of the normal microflora population overgrow if resistant to antibiotic you are taking

341
Q

How is antibiotic effectiveness tested?

A
  1. Kirby-Bauer test (diffusion susceptibility test => determines effectiveness in preventing microbial growth)
  2. MIC test (minimum inhibitory concentration test => determines drug potency, minimum concentration that can inhibit microbial growth)
  3. MBC test (minimum bactericidal concentration test => determines drug concentration required to kill microbe)
342
Q

What test determines drug potency?

A

MIC (minimum inhibitory concentration) test

343
Q

Describe the Kirby-Bauer diffusion susceptibility test.

A

1) Small disks of paper containing standard [drug]
2) Disks placed on surface of agar growth medium inoculated with the pathogen
3) Antimicrobial drugs diffuse through the agar
4) Zone of inhibition = growth inhibition seen around the disk
- The larger the zone of inhibition = the more effective the drug is
- Use standardized tables with properties of drugs and compare with zone of inhibition to see effectiveness of drug

344
Q

Describe the MIC (minimum inhibitory concentration) test.

A

1) Standardized amount of pathogen is added to a serial dilution of the antimicrobial agent in tubes/wells containing liquid growth medium
2) After incubation, turbidity in the medium indicates growth
- Determines drug potency = minimum [drug] that can inhibit growth
- The lower the minimum [drug], the more effective the drug is

345
Q

What is an Etest?

A

Combination of aspects of MIC & Kirby-Bauer tests:
1) Test strips with different concentrations of drug are put on a bacterial lawn
2) Determine minimum [drug] that can inhibit growth of the bacteria (don’t want higher [drug] because then side effects increase)

346
Q

Describe the MBC (minimum bactericidal concentration) test.

A

Determines amount of drug required to kill the microbe:
1) Samples taken from clear MIC tube or Kirby-Baeur inhibition zone
2) Transferred to plates containing drug-free growth medium
- Appearance of bacterial growth indicates bacteriostatic effect
- The lowest [drug] for which no growth occurs is the MBC

347
Q

What are some common routes of administration for antimicrobials?

A
  • Topical for external infections (drugs with high toxicity not as readily absorbed)
  • Oral (no needles, self-administered)
  • Intramuscular (drug via needle into muscle)
  • Intravenous (delivers drug directly to bloodstream => more preferred when infection in extremities)
348
Q

The drug’s route of administration affects…?

A
  • Drug distribution and concentration at the infected tissues (once in system, metabolized by kidney/liver)
  • Drug toxicities
349
Q

What drug is more toxic to the fetus in pregnant women? What is its effects?

A

Tetracyclines can cause:
- Malformation of skull
- Weakened & stained tooth enamel (forms complex with Ca++)

350
Q

What is the therapeutic index?

A

The ratio of the highest tolerable drug dose to the effective drug dose.
- Higher index = higher doses can be tolerated

351
Q

What is the therapeutic window?

A

The range of drug concentrations that are effective without being excessively toxic.

352
Q

What antibiotic are some individuals allergic to?

A

Penicillin (anaphylactic shock if taken)

353
Q

What microbes are associated with secondary infections and superinfections, as a result of antimicrobials causing a disruption of the normal microbiota?

A
  • Candida albicans (candidiasis)
  • Clostridium difficile (colitis)
354
Q

What are potential side effects of antimicrobial drugs?

A
  • Toxicity (to kidneys, liver, or nerves)
  • Allergic reactions
  • Disruption of normal microbiota
355
Q

Some pathogens are naturally resistant to drugs. Explain.

A
  • Selection pressure due to antibiotic use => develop resistance
  • The ones that are resistant outgrow the susceptible ones
356
Q

What are 2 ways bacteria acquire resistance to antimicrobial drugs?

A
  1. New mutations of chromosomal genes (may make the pathogen less susceptible)
  2. Horizontal gene transfer (transformation, transduction, and conjugation): acquisition of mutated genes or R plasmids that contain resistance gene
357
Q

R plasmids contain…?

A

Resistance gene

358
Q

What are the 3 ways horizontal gene transfer can occur?

A
  1. Transformation
  2. Transduction
  3. Conjugation
359
Q

What mechanisms do bacteria use to resist antimicrobials?

A
  • Enzyme production (e.g., β-lactamase) that destroys or activates drug
  • Slow or prevent drug entry into cell (e.g., capsules attached to cell surface)
  • Alter drug targets (so it binds less effectively)
  • Alter their own metabolic chemistry (e.g., get folic acid from environment instead of making it)
  • Efflux pumps (pump drug out of cell before it can act)
  • Biofilms (delay diffusion of drug into cells = [drug] kept at minimum)
360
Q

What does Mycobacterium tuberculosis produce to resist antimicrobials?

A

Produces MfpA protein that binds to DNA gyrase = prevents binding of fluroquinolone drug.

361
Q

What microbe is more prone to develop drug resistance to others?

A

Staphylococcus aureus

362
Q

What is multiple resistance? Where does it usually develop?

A
  • Multiple resistance = pathogen can acquire resistance to more than one drug
  • Common when R plasmids exchanged
  • Develops in hospitals and nursing homes (constant use of drugs eliminates sensitive cells)
363
Q

What are multiple-drug-resistant pathogens? What are they also called?

A

Bacteria resistant to at least 3 antimicrobial agents (superbugs).

364
Q

_______ resistance can occur when drugs are similar in structure (or have common pathway).

A

Cross resistance

365
Q

What strategies help slow antimicrobial resistance?

A
  • Maintain high [drug] in patient for sufficient time (to eliminate all pathogens before they give rise to resistant strains)
  • Use antimicrobial agents in combination
  • Use antimicrobials only when necessary
  • Develop new variations of existing drugs (2nd/3rd generation drugs)
  • Search for new antibiotics, semisynthetics, and synthetics (e.g., bacteriocins)
366
Q

_____________ occurs when one drug enhances the effect of a second drug.

A

Synergism (additive)

367
Q

Give examples of drug synergism.

A
  • Penicillin + Streptomycin => inhibition of cell wall by penicillin makes it easier for streptomycin to enter bacterial cells
  • Calvulanic acid enhances Penicillin effect by inhibiting β-lactamase
368
Q

Antibacterial proteins used by some bacteria to inhibit other bacterial strains.

A

Bacteriocins

369
Q

Normal/indigenous microbiota/flora are organisms that…?

A

Organisms that colonize the body’s surface without normally causing disease.

370
Q

The microbiome begins to develop during ________ process and much of it is established during _______________ of life.

A
  • Birthing process
  • First months of life
371
Q

Describe resident microbiota.

A
  • Part of the normal microbiota throughout life (e.g., re-establish colonies after showering)
  • Are mostly commensal
372
Q

Describe transient microbiota.

A
  • Remain in the body for short period
  • Found in the same regions as resident microbiota
  • Cannot persist in the body (competition, immune system, body chemical/physical changes)
373
Q

Why cannot transient microbiota persist in the body?

A
  • Competition from other microorganisms
  • Elimination by the body’s defense cells
  • Chemical or physical changes in the body (e.g., during menstrual cycle = vagina’s pH changes)
374
Q

Where are resident microbiota found in the body?

A
  • Respiratory tract (nose, trachea, bronchi) => NO microbiota in alveoli
  • Upper digestive tract (teeth, gingiva, lining of cheeks, pharynx, saliva)
  • Lower digestive tract (intestines) => bacteria mostly strict anaerobes
  • Urinary & reproductive tract
  • Skin (dead skin layers, hair follices, pores of glands) => not best/suitable environment because dry, gets washed constantly
  • Eyes => tears wash most microbiota from eyes
375
Q

What are opportunistic pathogens?

A

Normal microbiota that cause disease under certain circumstances.

376
Q

What are some conditions that trigger opportunistic pathogens?

A
  • Introduction into unusual site in body
  • Immune suppression (diseases, malnutrition, stress, aging, radiation, chemotherapy, immunosuppressive therapy)
  • Changes in the normal microbiota
  • Stressful conditions can disrupt normal microflora (physical/emotional stress, hormonal changes, diets)
377
Q

Esherichia coli (E.coli) is a normal flora in the colon, but if enters the _______, it can cause ____________.

A
  • Urethra
  • Urinary tract infection (UTI)
378
Q

Microbial ___________ and ___________ prevents opportunistic pathogens to cause disease.

A
  • Antagonism
  • Competition
379
Q

AIDS patients often die of ____________________.

A

Opportunistic infections (because HIV infection suppresses the immune system)

380
Q

What are reservoirs of infection? Why?

A

Sites where pathogens are maintained as a source of infection.
- Why? Most pathogens cannot survive for long outside their host

381
Q

What are the 3 types of reservoirs of infection?

A
  1. Animal reservoir (zoonoses)
  2. Human carriers (asymptomatic, healthy carriers)
  3. Nonliving reservoir (contaminated soil, water, food => through feces/urine)
382
Q

What are zoonoses? How are they acquired?

A
  • Spread of disease from animals to humans (animal reservoir)
  • Acquire through various routes: direct contact with animal or its waste, eating animals, etc.
383
Q

What are healthy human carriers?

A
  • Asymptomatic but infective individuals
  • Some individuals eventually develop illness, others not
384
Q

What virus causes rabies?

A

Lyssavirus species

385
Q

What is the difference between contamination vs. infection?

A
  • Contamination = the mere presence of microbes in or on the body (does not always lead to an infection)
  • Infection = when organism evades body’s external defenses, multiplies, and becomes established in the body
386
Q

What are the 4 portals of entry through which pathogens enter the body?

A
  • 3 major pathways: skin, mucous membranes, placenta
  • Parenteral route circumvents the usual portals (not natural)
387
Q

Describe the skin’s role in infection.

A
  • Outer layer of dead skin cells (epidermis) acts as a barrier to pathogens => water permeable, dry
  • Sweat and oils (sebum) secreted on the skin may have antimicrobial properties
  • Some pathogens can enter through openings or cuts
  • Larvae of some parasitic worms can burrow into the skin
  • Some fungal pathogens can digest outer layers of skin (produce certain enyzmes)
388
Q

Describe the roles of mucous membranes in infection.

A
  • Line the body cavities that are open to the environment (respiratory, GI, urinary, reproductive tracts)
  • Provide a moist, warm environment hospitable to pathogens
  • Presence of layer mucus, antimicrobial peptides, acidic stomach pH, mucosal immune system, and normal microbiota provide a barrier to infectious microbes
389
Q

________________ is the most common site of entry for pathogens.

A

Respiratory tract (entry through nose, mouth, or eyes)

390
Q

What are the barriers to infection found in mucous membranes?

A
  • Mucus (secreted by goblet cells)
  • Antimicrobial peptides
  • Acidic stomach pH
  • Mucosal immune system
  • Normal microbiota
391
Q

What are the components of mucous membranes?

A
  • Mucus (secreted by goblet cells)
  • Epithelium
  • Basement membrane
  • Lamina propria (connective tissue, blood vessels, nerves, immune cells)
392
Q

Describe the placenta’s role in infection.

A
  • Typically forms effective barrier to pathogens (even normal microbiota)
  • Pathogens may cross the placenta and infect the fetus => spontaneous abortion, birth defects, or premature birth
393
Q

What are some pathogens that can cross the placenta?

A
  • Toxoplasma gondii (protozoan)
  • Treponema pallidum, Listeria monocytogenes (bacteria)
  • Cytomegalovirus, Erythrovirus (DNA viruses)
  • HIV/Lentivirus, Rubivirus (RNA viruses)
394
Q

What is the parenteral route of entry?

A
  • Puncture of skin or mucous membranes by contaminated nail, thorn, hypodermic needle
  • Accidental/unintentional exposure (NOT a true portal of entry)
395
Q

What is adhesion?

A
  • Adhesion = process by which microorganisms attach themselves to cells/tissues
  • Required to establish colonies successfully within the host
  • Pathogens use adhesion factors for attachment to tissues
396
Q

What are some adhesion factors (adhesins) pathogens use for attachment to tissues?

A
  • Specialized structures (e.g., suckers and hooks in some helminths)
  • Attachment molecules (e.g., glycoproteins, biofilms)
397
Q

__________ on the surface of viruses and bacteria bind to receptors on host cells. They determine _____________.

A
  • Glycoproteins
  • Determine tissue or host specificity
398
Q

Sticky web of bacteria and polysaccharides, called a _________, such as dental plaques.

399
Q

Some pathogens may have more than one type of adhesin, while others may change adhesin over time. Provide examples of each.

A
  • More than one = Bordetella (whooping cough)
  • Change over time = Plasmodium (malaria)
400
Q

Infectious disease results if the invading pathogen alters normal body function; also referred to as __________.

401
Q

Etiology is the study of the cause of disease. What are some categories of diseases?

A
  • Hereditary (genetic)
  • Congenital (birth defects)
  • Degenerative (aging of cells)
  • Nutritional
  • Endocrine (hormonal)
  • Mental (emotional/psychosomatic)
  • Immunological (hyper/hypoactive immunity)
  • Neoplastic (tumour)
  • Infectious
  • Iatrogenic (medical treatment/procedure => surgical error)
  • Idiopathic (unknown cause)
  • Nosocomial (healthcare-associated)
402
Q

“Hepat-“ refers to the?

403
Q

“Terato-“ refers to?

404
Q

“Septi-“ refers to?

A

Rotting (presence of pathogens)

405
Q

What ways can diseases be classifed?

A
  • Taxonomic categories
  • Affected body system
  • Longevity (acute vs. chronic)
  • Severity
  • How they spread (local vs. systemic)
  • The effects they have on populations
406
Q

Disease transmitted from one host to another.

A

Communicable disease

407
Q

What is the difference between acute vs. chronic disease?

A
  • Acute = symptoms develop rapidly, last shortly
  • Chronic = mild symptoms that develop slowly and last a long time
408
Q

What is a focal infection?

A

Infection site that serves as a source of pathogens for infections at other sites in the body.

409
Q

What is the difference between symptoms vs. signs?

A
  • Symptoms = subjective characteristics of disease felt only by the patient (pain, nausea, headache, etc.)
  • Signs = objective manifestations of disease observed or measured by others (swelling, redness, vomiting, diarrhea, fever, etc.)
410
Q

Symptoms and signs that characterize a disease or an abnormal condition.

411
Q

___________________ infections lack symptoms but may still have signs of infections.

A

Asymptomatic or subclinical

412
Q

Germ theory of disease was developed by ____________.

A

Louis Pasteur (infections by microbes cause disease)

413
Q

Robert Koch studied etiology and showed that…?

A
  • Bacillus anthracis causes anthrax
  • Mycobacterium tuberculosis causes tuberculosis
414
Q

Koch’s postulates are a series of…?

A

A series of essential conditions that scientists must demonstrate or satisfy to prove that particular microbe causes a particular disease.

415
Q

What are exceptions to Koch’s postulates?

A
  • Some pathogens can’t be cultured in the lab
  • Some diseases caused by combination of pathogens and other cofactors
  • Ethical considerations (e.g., pathogens that require a human host)
416
Q

What is pathogenicity?

A

Ability of a microorganism to cause disease.

417
Q

What is virulence?

A

Microorganism’s degree of pathogenicity (ability to cause disease).

418
Q

What are some virulence factors?

A
  • Adhesion factors
  • Biofilms
  • Extracellular enzymes
  • Toxins
  • Antiphagocytic factors
419
Q

Francisella tularensis (rabbit fever) is more/less virulent than Candida albicans (vaginitis).

A

More virulent

420
Q

Describe extracellular enzymes (virulence factors). Give examples.

A
  • Secreted by pathogens to dissolve structural chemicals in the body
  • Help pathogen maintain infection, invade, and avoid body defenses
  • Examples: hyaluronidase (Clostridium perfringens), collagenase (Clostridium & Streptococcus), keratinase (ringworm fungi => Trichophyton, Microsporum, Epidermophyton), mucinase (Entamoeba histolytica), kinase (Streptococcus & Staphlyococcus), coagulase
421
Q

Secreted by pathogens to dissolve structural chemicals in the body.

A

Extracellular enzymes

422
Q

Hyaluronidase is secreted by…?

A

Clostridium perfringens (digest hyaluronic acid = polysaccharide, glue-like structure that holds cells together)

423
Q

Collagenase is secreted by…?

A

Clostridium & Streptococcus species (digest collagen = major matrix protein that gives tissues structure)

424
Q

Keratinase is secreted by…?

A

Fungi that cause ringworm => Trichophyton, Microsporum, Epidermophyton floccosum (digest keratin = protein in skin, hair, nails)

425
Q

Mucinase is secreted by…?

A

Entamoeba histolytica (digest mucus to attach to mucous membranes)

426
Q

Kinase is secreted by…?

A

Streptococcus & Staphylococcus species (digest blood clot to enter bloodstream and spread)

427
Q

Pathogens that secrete coagulase cause…?

A

Formation of blood clot:
- Pathogen lives inside to protect themselves from immune cells
- Digest clot when time is right

428
Q

Chemicals that harm tissues or trigger host immune responses that cause damage.

429
Q

Toxemia refers to…?

A

The presence of toxins in the bloodstream.

430
Q

What are the 2 types of toxins?

A
  1. Exotoxins (cytotoxin, neurotoxin, enterotoxin)
  2. Endotoxin (Lipid A)
431
Q

Endotoxins are only produced by…?

A

Gram-negative bacteria

432
Q

What are some examples of exotoxins?

A
  • Cytotoxin (kill host cells)
  • Neurotoxin (affect nerve cell function)
  • Enterotoxin (affect cells of the GI tract => e.g., excess release of fluids)
433
Q

Enterotoxins (type of exotoxin) affect cells of the…?

434
Q

Cytotoxins (type of exotoxin) kill…?

A

Host cells

435
Q

What is an example of an endotoxin?

A
  • Lipid A component of LPS from Gram-negative bacteria
  • Released upon cell death
  • Causes fever, inflammation, blood coagulation, shock, etc.
436
Q

What is something that causes fever called?

437
Q

What are toxoids?

A

Inactivated forms of toxins (used for vaccination).

438
Q

Describe some general characteristics of exotoxins.

A
  • Metabolic product (protein or short peptide) secreted from living cell
  • Mainly Gram-positive and Gram-negative bacteria
  • High toxicity
  • Typically unstable > 60C
  • Non-pyrogenic
  • Strong antigenicity (stimulate antibody production)
  • Toxoid formation with heat or formaldehyde
439
Q

Describe some characteristics of endotoxins.

A
  • Gram-negative bacteria
  • Lipid A of LPS
  • Low toxicity (can be more at higher concentrations)
  • Stable for up to 1 hour at autoclave temp (121C)
  • Pyrogenic
  • Weak antigenicity
  • Don’t form toxoids
440
Q

What are some representative diseases associated with exotoxins?

A
  • Botulism (Clostridium botulinum)
  • Tetanus (Clostridium tetani)
  • Gas gangrene (Clostridium perfringens)
  • Diphtheria (Corynebacterium diphtheriae)
  • Cholera (Vibrio cholerae)
  • Plague (Yersinia pestis)
  • Staphylococcal food poisoning
441
Q

What are some representative diseases associated with endotoxins?

A
  • Typhoid fever (Salmonella typhi)
  • Tularemia (Francisella tularensis)
  • Endotoxic shock
  • UTIs
  • Meningococcal meningitis
442
Q

_______________ factors prevent phagocytosis by the host’s phagocytic WBCs (macrophages and neutrophils).

A

Antiphagocytic factors

443
Q

What are some antiphagocytic factors?

A
  • Bacterial capsules => composed of chemicals not recognized as foreign (e.g., hyaluronic acid capsule)
  • Antiphagocytic chemicals (Neisseria gonorrhoeae) => prevent fusion of lysosome and phagocyte
  • M protein (Streptococcus pyogenes) => inhibits phagocytosis
  • Leukocidins => directly destroy phagocytic cells
444
Q

What bacteria produces M protein to inhibit phagocytosis?

A

Streptococcus pyogenes

445
Q

__________ directly destroy phagocytic cells.

A

Leukocidins

446
Q

What allows Neisseria gonorrhoeae to survive inside phagocytes?

A

Antiphagocytic chemicals (prevent fusion of lysosome and phagocyte)

447
Q

What are the 5 stages of infectious diseases following infection?

A

Can transmit disease at any stage:
1. Incubation period (no symptoms/signs => short if highly virulent)
2. Prodromal period (vague, mild general symptoms => e.g., tired, headache)
3. Illness (most severe signs and symptoms)
4. Decline (declining signs/symptoms => if medical intervention or immune response)
5. Convalescence (no signs/symptoms)

448
Q

Pathogens leave their host through multiple portals of exit often in materials the body secretes/excretes. Give examples.

A
  • Eyes (tears)
  • Ears (earwax)
  • Mouth (saliva)
  • Skin (blood, flakes)
  • Anus (feces)
  • Urethra (urine)
  • In males => seminal vesicles (semen)
  • In females => mammary glands (milk), vagina (blood, secretions)
449
Q

What is transmission or transmissible diseases?

A

The movement of pathogens from reservoir or a portal of exit to another host’s portal of entry.

450
Q

What are the 3 modes of transmission?

A
  1. Contact
  2. Vehicle
  3. Vector
451
Q

Describe the types of contact transmission.

A
  1. Direct contact transmission => involves body contact between hosts (can occur within a single individual too)
  2. Indirect contact transmission => pathogens are spread from host to host by fomites (drinking glasses, toothbrushes, etc.)
  3. Droplet transmission => spread of pathogens in droplets of mucus by exhaling, coughing, sneezing
452
Q

Describe the types of vehicle transmission.

A
  1. Airborne transmission => when pathogens travel more than 1m via an aerosol (via sneezing, coughing, AC systems, sweeping)
  2. Waterborne transmission => water contaminated with sewage (fecal-oral infection like cholera), important in the spread of GI diseases
  3. Foodborne transmission => spread of pathogens in/on foods (contaminated with feces, inadequately processed/cooked/refrigerated)
  4. Bodily fluid transmission => blood, urine, saliva can carry pathogens (prevent contact with conjunctiva, breaks in the skin, mucous membranes)
453
Q

Airborne transmission is when pathogens travel more than __ meter via an aerosol.

454
Q

Vector transmission can occur via…?

A
  • Biological vectors (e.g., biting arthropods => serve as host for some stage of pathogen’s life cycle)
  • Mechanical vectors (passive transport, not infected)
455
Q

Epidemiology allows us to gain important information on how to…?

A

Treat and prevent infectious diseases.

456
Q

Disease occurrence is tracked using what measures?

A
  • Incidence = # of new cases of a disease in a given area during a given period of time
  • Prevalence = # of total cases of a disease in a given area during a given period of time
  • Frequency (e.g., 1 in 100,000 individuals)
  • Geographic distribution (e.g., how dense are the cases in certain locations?)
457
Q

Number of new cases of a disease in a given area during a given period of time.

458
Q

Number of total cases of a disease in a given area during a given period of time.

A

Prevalence

459
Q

What are the 3 types of epidemiological studies?

A
  1. Descriptive epidemiology => tabulation of epidemiological data, identification of index case (the first case)
  2. Analytical epidemiology => retrospective: determines probable cause/mode of transmission/prevention methods
  3. Experimental epidemiology => tests hypothesis regarding disease cause, applies Koch’s postulates
460
Q

What is descriptive epidemiology?

A
  • Careful tabulation of epidemiological data concerning a disease (location/time of cases, patient information)
  • Main goal = source of disease (where it started, how it spread)
  • Identification of index case (the first case) important
461
Q

Why is identification of the index case (the first case of a disease) difficult or impossible?

A

Person could have recovered, moved, died, etc.

462
Q

What epidemiological study is useful in situations when Koch’s postulates can’t be applied?

A

Analytical epidemiology

463
Q

Describe analytical epidemiology.

A
  • Seeks to determine the probable cause, mode of transmission, and methods of prevent
  • Often retrospective (investigation occurs after an outbreak has occured)
  • Useful when Koch’s postulates can’t be applied
464
Q

Describe experimental epidemiology.

A
  • Tests a hypothesis concerning the cause of a disease
  • Application of Koch’s postulates
465
Q

The earliest known descriptive epidemiological study was by…? Describe it.

A
  • John Snow => studied 1854 cholera outbreak in London
  • Carefully mapped location of cases => found that they were clustered around the Broad street water pump
  • Determined disease spread via contamination of drinking water by sewage
466
Q

Describe the various ways epidemiologists report data.

A
  • Average annual incidence on a map of a geographical area
  • Graphs (% of cases by week of onset, # of deaths by age)
467
Q

What does “endemic” mean?

A

Disease that occurs continually and stably within in area (e.g., Sub-Saharan Africa endemic for malaria).

468
Q

Disease that occurs in low numbers in an area is called…?

469
Q

What is the difference between an epidemic and pandemic?

A
  • Epidemic = disease occurrence is higher than expected in an area
  • Pandemic = epidemic in more than one continent
470
Q

Epidemics are not defined according to the absolute number of cases, but…?

A

How much it exceeds the expected occurrence in an area (e.g., epidemics may have fewer cases than non-epidemics).

471
Q

What is needed for epidemiological classification?

A
  • Good recording of disease prevalence in area or population
  • E.g., healthcare providers are required to report certain infectious diseases to their local, state/provincial, and national health departments
472
Q

_________________ are required to report certain infectious diseases to their local, state/provincial, and national health departments.

A

Healthcare providers

473
Q

What are nosocomial infections? What are the different types?

A

Healthcare-associated infections (acquired by patients while they are in a healthcare setting):
- Exogenous => pathogen acquired from healthcare environment
- Endogenous => pathogen arises from patient’s normal microbiota
- Iatrogenic => results from medical procedures (surgery, catheters, intubation, hypodermic needles)
- Superinfections => use of antimicrobial drugs inhibits some resident microbiota, allowing other microbes to thrive

474
Q

What are factors influencing nosocomial infections?

A
  • Exposure to numerous pathogens in a healthcare setting, including drug-resistant strains
  • Weakened immune system of patients
  • Transmission among healthcare providers, patients, and visitors
475
Q

What are ways to control nosocomial infections?

A
  • Medical asepsis (good housekeeping, hand washing, sanitary food handling, proper hygiene, etc.)
  • Personal protective equipment (PPE = masks, gloves, gown, etc.)
476
Q

What are some Canadian public health organizations?

A
  • Health Canada
  • Public Health Agency of Canada (PHAC)
477
Q

What are some American public health organizations?

A
  • National Public Health Agency
  • Centers for Disease Control (CDC)
478
Q

What organization coordinates public health efforts worldwide?

A

World Health Organization (WHO)

479
Q

How do public health agencies work to limit or interrupt disease transmission?

A
  • Enforce cleanliness of water and food supplies
  • Work to reduce disease vectors and reservoirs
  • Establish and enforce immunization schedules
  • Locate and treat individuals exposed to contagious pathogens
  • Establish isolation and quarantine measures
  • Educate the public on healthy choices to limit diseases (e.g., STDs)
480
Q

Why is it necessary to maintain a high drug concentration for sufficient time in a patient when treating an infectious disease?

A

Ensures that all the bacteria, including any that may have slower growth rates, are exposed to the drug, preventing the survival and potential development of resistant strains.