Intro Flashcards

1
Q

Name the 7 types of microorganisms

A

Bacteria, fungi, viruses, protozoa, algae, archaea, multicellular animal parasites

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2
Q

What classification system exists for viruses? How does replication differ between the classes?

A

The Baltimore system; class 1 + 2 replicate within the nucleus, class 3-7 replicates in the cytoplasm

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3
Q

Explain how gram staining works

A
  1. the iodine in the crystal violet stain precipitates and binds to the peptidoglycan layer
  2. Add alcohol and wash away the stain, the thin peptidoglycan layer of gram (-) bacteria is so thin it washes away and remains colourless, but the thick peptidoglycan layer of gram (+) remains purple
  3. Add a pink counterstain, leaving the (-) bacteria pink and the (+) blue
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4
Q

What are the structural differences between gram (-) and (+) bacteria

A

Gram (-) has a thin peptidoglycan layer and a lipopolysaccharide layer which holds antibodies

Gram (+) has a thick peptidoglycan layer and no lipopolysaccharide layer

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5
Q

What stain would you use to identify mycobacterium and why?

A

Z-N stain as the mycolic acid prevents the crystal violet stain from washing away

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6
Q

Contrast the terms pathogenicity and virulence, what determines them?

A

Pathogenicity is the ability of a microorganism to cause disease and damage and virulence is the degree of pathogenicity. They are both determined by the composition of the genome, virulence can also depend on how the bacteria entered the host

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7
Q

Contrast the terms parasite and pathogen

A

A parasite is an organism that can live on or within a secondary organism/’host’, a pathogen is an organism that can cause damage to the host

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8
Q

What is a plasmid?

A

An extra piece of DNA often carrying the bacteria’s virulent factors

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9
Q

Define attenuation

A

When a pathogen’s virulence is reduced

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10
Q

What 5 key steps do virulence factors help bacteria to do? (ACITI)

A
  1. Attach to the host (Via adhesins)
  2. Colonization (and enzymes)
  3. Invade
  4. Toxins (and enzymes) aid deeper penetration to avoid host defences
  5. Inhibit phagocytosis
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11
Q

Define the following terms:

a) Toxin
b) Toxigenicity
c) Toxemia
d) Toxoid
e) Antitoxin

A

Toxin: substances produced by pathogens that contribute to pathogenicity

Toxigenicity: ability to produce a toxin

Toxemia: Presence of toxin in the host’s blood

Toxoid: inactivated toxin used in a vaccine

Antitoxin: antibodies against a specific toxin

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12
Q

What are the 2 types of toxins and what is their key difference?

A

Exotoxins are proteins produced/secreted by bacteria and endotoxins are within the bacterial composition

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13
Q

Where and when are endotoxins released? Why are they so damaging?

A

Endotoxins are released from the lipid portion of the outer membrane (lipid A) from gram (-) bacteria either when…

a) a gram (-) bacteria dies and releases it or
b) when a gram (-) bacteria is engulfed by the immune system and the debris (broken up parts of the lipid) is expelled by the macrophage and free to circulate in the system

Endotoxins are highly antigenic and provoke a strong immune response, quickly causing heightened inflammation, fever and possible shock

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14
Q

Who releases exotoxins?

A

By both gram-positive and negative bacteria, but all major gram-positive will produce it

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15
Q

Describe how each of the three types of exotoxins cause damage/dysfunction

A

Type 1: Signalling at the host cell

Type 2: Damaging the membrane/phospholipid bilayer by making protein channels in it

Type 3: Entering the target cell and directly altering the function

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16
Q

Name the 3 classes of toxins

A
  1. Neurotoxin (acts on nervous system)
  2. Enterotoxin (acts on gut)
  3. Superantigen
17
Q

What is a superantigen? Why are they so damaging? Name 4 symptoms of being infected with a superantigen (+1 very bad symptom)

A

A Type 1 exotoxin, they are unspecific and bind to any T cell which releases cytokines causing a heightened intense immune response = nausea, vomiting, fever, shock and death

18
Q

Which superantigen causes TSST and name 3 major signs

A

Toxic shock syndrome toxin is caused by TSST-1. Causes hypotension, organ dysfunction and desquamative (peeling) skin lesions

19
Q

Name 5 symptoms of scalded skin syndrome. What bacterium causes it/how?

A

Caused by staphylococcus aureus which produces an exfoliating toxin causing the outer layers of skin to blister and peel

Symptoms: fever, redness, skin exfoliation, skin wrinkles and blisters/lesions

20
Q

How can clostridium lead to gas gangrene?

A

Since clostridium are type 1 exotoxins, they damage the membrane and increase the permeability of blood vessels, damaging the bloodflow and allowing gas to get into the tissue

21
Q

Why are clostridia spore-forming?

A

Since they’re anaerobic and particular about where they grow, they create spores as a protective mechanism so they can withstand environments they can’t grow in (aerobic)

22
Q

Describe the size, shape, type (-) or (+), environmental niche and protective features of a clostridia

A

Large, bacilli, gram (+), anaerobic, spore forming

23
Q

Explain how the ‘A’ and ‘B’ segment of an A-B enterotoxin work together to infect

A

The B is the binding part of the toxin, the A part is active and can then be incorporated into the host cell. The B part then dissociates and is recycled out, while A stays and infects

24
Q

Describe the mechanism of the cholera toxin

A

Acts on intestinal epithelia and stimulates adenyl cyclase activity, water and sodium ions pass into the gut and you have watery diarrhea

25
Q

Describe the basic mechanism of the tetanus toxin

A

A-B neurotoxin: Blocks the inhibitory neurons causing continual muscle contractions

26
Q

How do pili influence the immune system?

A

They are antigenic and produce a response from the immune system

27
Q

What is LD50?

A

The legal dose to kill half the bacteria

28
Q

What is microbiota and a microbiome?

A

A microbiota is a community of microorganisms living in a specific environment, a microbiome is a collection of specific microbiota

29
Q

Describe the 2 types of transmission

A

Vertical: acquisition of microbes directly from a parent

Horizontal: acquisition of microbes from environment and non-parental factors (i.e diet and nutrition)

30
Q

What are 2 ways vertical transmission may occur?

A

Vaginal: labour, rupture of membranes, bacteria may travel up vagina to amniotic fluid, transfer as baby goes down birth canal, aspirate into baby’s lungs

Gut: fetus comes in contact with mother’s faecal matter during birth process

31
Q

Describe the bacteria Group B streptococcus, where does it commonly colonize? In what population can it cause serious disease?

A

Gram (+), beta hemolytic, commonly colonizes in GI and genitourinary tract. Largely affects infants, pregnant women and older adults

32
Q

What are 4 additional risk factors for early onset GBS disease?

A
  1. Obstetric: preterm delivery, prolonged membrane rupture, infection/fever during labour
  2. GBS in mother’s urine during pregnancy
  3. Previous infant with GBS disease
  4. Low maternal levels of anti-GBS antibodies
33
Q

Name the 5 stages of biofilm formation

A

Stage…

  1. Initial attachment
  2. Irreversible attachment
  3. Maturation
  4. Maturation II: now initial base organisms are protected and can avoid the host immune system
  5. Dispersion (going off to form another biofilm in close proximity)
34
Q

Define the term dysbiosis

A

The persistent imbalance of the gut’s microbial community which can relate to many diseases all over the body

35
Q

What might you do if you suspected a patient has an imbalance in their gut flora?

A

Order a breath test, have individual drink a high glucose drink and measure amount of methane produced over time

Begin them on an antimicrobial program

36
Q

What is one con to beginning an antimicrobial program?

A

Antibiotics are unspecific and will take out large amounts of natural protective bacteria, allowing opportunistic bacteria to flourish