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PMP-101 > Microbe-host interactions: Microbiota and pathogens > Flashcards

Microbe-host interactions: Microbiota and pathogens Flashcards

1
Q

What are symbolic relationships?

A

when there are close interaction between two organisms of different species

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2
Q

Name the 3 types of symbiotic reletionships:

A

1) Mutualism
2) Commensalism
3) Parasitism

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3
Q

1) Bacteria – Host interactions: Mutualism

A

Both species (bacteria and host) benefit from their interactions

Benefit to the bacteria > They have a place to eat, survive and multiply

Benefits to the human > Bacteria aid digestion, breaking down food that the host cannot normally digest and producing vitamins (such as B and K)

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4
Q

2) Bacteria – Host interactions: Commensalism

A

One partner in the relationship benefits. The other neither benefits nor is harmed.

Benefit to the bacteria > Acquire nutrients consuming dead skin and a place to live and grow

Commensal bacteria may become pathogenic = disease

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5
Q

3) Bacteria – Host interactions: Parasitism

A

One partner, the pathogen, harms the host, causing infectious disease

Benefit to the virus > Virus takes advantage of the translational machinery of the cell to replicate (multiply) virus particles. Viruses = obligate intracellular parasites

Harm for the human cells > Viral infections = death of the cells and tissue damage

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6
Q

example of Mutualism:

A

Many hundreds of bacterial species living in the gut (gut microbiota/flora)

The human gut harbours trillions of microbes in healthy conditions

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7
Q

example of Commensalism:

A

Commensal bacteria colonise epithelial surfaces of skin 1 million bacteria on each square centimeter (cm2)

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8
Q

example of Parasitism:

A

SARS-CoV-2 infects human cells of the respiratory system, causing COVID-19

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9
Q

What is Microbiota

A

all the microorganisms that live in and on an organism

Approximately 1011 organisms
1-3% total body mass
Generally non-pathogenic
Symbiotic with host

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10
Q

EARLY colonization:

A
  1. Microbiota begins developing at birth
  2. Vaginal birth = exposure to microbes from the mother’s birth canal, whereas caesarean delivery = microbe exposure from initial caretakers
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11
Q

Bifidobacteria are important coloniser of the gut.
Ferment what?

A

sugars found in human breast milk provides the infant with calories and lowers the gut pH, limiting growth of pathogens

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12
Q

Dynamic and diverse microbiota composition

A

Microbiota is not static

It reach a adult-like composition by age 3

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13
Q

microbiota composition in adults

A

stable - without any major physical or lifestyle changes

vary from person

not only bac = some archaea, fungi, viruses present

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14
Q

Human microbiota body sites
determined by many factors:

A

Nutrients
Physical and chemical factors
Host defenses
Mechanical factors

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15
Q

do Internal organs and tissues (that is, brain, blood, cerebrospinal fluid, muscles) contain microorganisms

A

not normally

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16
Q

Distribution of microbiota niches (skin and mucous membranes) in the human body

A
  • eyes
    -mouth
  • nose and throat
  • lungs
  • skin
  • stomach
  • large intestine
  • small intestine
  • urogenital tract
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17
Q

What are the human microbiota functions?

A
  1. Dietary fibre fermentation (resistant to host enzymes) into Short Chain Fatty Acids (source of energy)
  2. Synthesise and excrete vitamins (vit. K and B12)
  3. Prevent .colonisation by pathogens - competitive exclusion of pathogens/ production or stimulation of antimicrobial molecules
  4. Stimulate the development of certain tissues (intestines, lymphatic tissues, capillary density)
  5. Immune system stimulation/maturation
  6. Regulate inflammation
  7. Modulate and affect the central nervous system (Gut-Brain Axis)
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18
Q

Dysbiosis

A

refers to an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes

19
Q

what causes dysbiosis and what can it lead to?

A
  • dietary changes
  • antibiotic use
  • psychological and physical stress

> > inflammation

20
Q

Opportunistic infections

A

infection caused by commensals (part of the normal microbiota) that do not cause generally disease in a healthy host

21
Q

Dysbiosis – altered microbiota
what can pathogen do?

A

outgrow

22
Q

Probiotics -

A

Live microorganisms, which, when administered in adequate amounts, can restore the normal balance of microbiota (especially in the gut and genital) and related beneficial functions, conferring a health benefit to the host.

23
Q

Prebiotics

A

compound(s) added to enhance the colonization and positive health benefits of probiotic microbes.

24
Q

Synbiotics

A

foods or supplements that include both a prebiotic and a probiotic.

25
Q

Pathogen

A

Any organism that causes disease

26
Q

Opportunistic pathogen

A

may be part of normal microbiota and causes disease when the host is immunocompromised or when they have chance to outgrowth

27
Q

Pathogenicity

A

Ability of a pathogen to cause disease

28
Q

Virulence

A

Degree of harm (pathogenicity) inflicted on its host

29
Q

What are the 6 steps of Steps in pathogenesis of bacterial infections?

A
  1. Entry of pathogens into the body
    Any organism that causes disease according to the transmission routes (e,g. penetration, inhalation, ingestion and introduction into the blood)
  2. Attachment of the pathogen to some tissues
  3. Multiplication
  4. Invasion/spread of the pathogen
  5. Evasion if the host defences/immunity
  6. Damage to the host tissue(s)
30
Q

3 steps; Entry, adherence and colonisation:

A
  1. Entry into the host
    Portal of entry
    Skin, respiratory, gastrointestinal, urogenital systems, or conjunctiva of eye
  2. Attachment of microbe to target cell is first (high degree of specificity)
    Adherence structures:
    Pili
    Fimbriae
    Glycocalyx (Capsule)
  3. Colonisation—establish a site of microbial replication on or within host
31
Q
  1. Invasion (entry, adherence and colonisation)
A

Active - occurs through production of lytic substances that alter host tissue
E.g. pathogens that induce the disruption of the intestinal lining

Passive – host tissue alteration was already present and it was not caused by the pathogen
skin lesions, insect bites, wounds

32
Q

examples of invasion

A

Once under mucous membrane, a pathogen can penetrate deeper tissues

Bacteremia—presence of viable bacteria in the blood

Septicemia—bacterial or fungal toxins in the blood

33
Q

invasion varies among pathogens;

A

Clostridium tetani (tetanus) is noninvasive because it does not spread from one tissue to another, but toxins become blood borne

Bacillus anthracis (anthrax) and Yersinia pestis (plague) also produce toxins and are highly invasive

Streptococcus span invasiveness

34
Q

Overcoming Host Defences
step 5

A

Successful pathogens overcome competition and elude initial host responses as well as the adaptive immune system:

35
Q
  1. overcoming host defences
    bullet points
A

Find shelter to avoid recognition by defence cells.
Survive and replicate inside host cells
Squeeze between host cells.
Avoid phagocytosis (capsule)
Burrow under mucus.
Find shelters within biofilms.
Produce enzymes that inactivate innate resistance mechanisms.
Excrete specialized proteins to selectively kill host cells
Mutate and/or reduce cell surface proteins detected by immune cells

36
Q

Overcoming Host Defences - examples

A

Bacteria such as Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae produce a slippery mucoid capsule that prevents phagocytosis by host immune cells

Eliminate O-antigen on lipopolysaccharide (LPS) to diminish immune recognition and clearance

Biofilm bacteria are protected from antimicrobial agents, antibody and host immune cell, as shown in the Figure

37
Q
  1. Damage to the host tissue(s)
A

secreting enzymes that degrade host cell for nutrients

replicating inside cells, inducing apoptosis of the immune cell

Toxins – substances that disrupt the normal metabolism of host cells
- Exotoxins
- Endotoxins

Hypersensitivity reactions - excessive release = cytokines by immune cells and exacerbating inflammatory responses, destroying tissues

38
Q

Types of toxins

A

Exotoxins
Endotoxins

39
Q

Exotoxins

A

produced inside mostly gram +ive bacteria as part of their growth and metabolism

released into surrounding medium

40
Q

Endotoxins

A

part of outer portion of cell wall (lipid) of gram -ive bacteria

liberated when bacteria die and cell wall breaks apart

41
Q

antimicrobial chemotherapy

A

administration of specific drug to treat infectious disease, having selective toxicity against pathogens involved in infections, not host cells

42
Q

selectivity

A

take advantage of the difference between structure of the bacterial cell and the host’s cell

43
Q

recap - fatty acids broken down

A

Fatty acid oxidation is the mitochondrial aerobic process of breaking down a fatty acid into acetyl-CoA units.
Fatty acids move in this pathway as CoA derivatives utilizing NAD and FAD.

Fatty acids are activated before oxidation, utilizing ATP in the presence of CoA-SH and acyl-CoA synthetase

PMP-101 (53 decks)

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