Bacterial Properties and Disease Flashcards

Bacterial properties: explain the meaning of the following terms when describing bacterial structure and function; coccus, bacillus, rod, Gram-negative, Gram-positive, acid-fast, aerobic, anaerobic, intra-cellular, extra-cellular Bacterial gene transfer: compare the three main ways bacteria use to exchange genetic material Infectivity and virulence: explain the concepts of infectivity and virulence, and define the term infective dose Bacterial sources and routes: list the potential sources an (46 cards)

1
Q

Features of bacteria?

A

Small, unicellular. No internal membrane-bound organelles. Haploid. Some have flagella.

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2
Q

Three bacterial forms?

A

Cocci bacteria – spherical Bacilli – rod shaped Spirilli – spiral

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3
Q

What is Gram stain used for, and how is it done?

A

Gram stain technique distinguishes between two different cell wall types. Stained with violet dye and iodine, rinsed in alcohol, stained with red dye.

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4
Q

What are the results of Gram stain that enable us to distinguish type of bacteria? Why, briefly, do each retain/not retain stain?

A

Gram-positive bacteria retain dye in because of peptidoglycan in cell wall. High peptidoglycan = deep violet. Gram-negative bacteria lose dye because of thinner peptidoglycan and presence of outer membrane. Cells absorb counterstain making them pink.

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5
Q

Structure of Gram-positive and Gram-negative bacteria? What does LPS do?

A

Gram positive = single membrane Cell wall is on extracellular surface which contain peptidoglycan and other proteins. Gram negative = double membrane Periplasm sandwiched between membranes contains peptidoglycan. Extracellular part of cell wall is predominantly lipopolysaccharide (or LPS) – extremely potent for our innate immune system. Immune system receptors are very sensitive to LPS – initiating pro-inflammatory response. So LPS can be dangerous in high quantities.

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6
Q

Name 5 pathogenic Gram negative bacteria?

A

Escherichia coli (diarrhea, dysentery, kidney failure) Salmonella (‘-typhimurium’ – food poisoning, or ‘-typhi’ – typhoid) Shigella (dysentery – inflammatory disease of intestines) Vibrio cholerae (cholera) Neisseria (‘-meningitidis’ – meningitis, or ‘-gonorrhoeae’ – gonorrhoea)

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7
Q

Name 4 pathogenic Gram positive bacteria?

A

Staphylococcus aureus (skin diseases, joint diseases, pneumonia)
Streptococcus pneumoniae (pneumonia, meningitis)
Streptococcus pyogenes (tonsilitis, necrotizing fasciitis (flesh-eating bacteria)).
Clostridium (difficile).

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8
Q

What are Myobacteria? Name 2 bacteria?

A

Evolutionary distinct from Gram +/-. Mycobacterium tuberculosis (TB) Mycobacterium leprae (leprosy)

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9
Q

What do bacterial pathogens need to be adapted for?

A

CPR in Washington DC Adapted to colonize (surface structures), Persist (avoid host defences), Replicate (acquire nutrients through complex mechanisms e.g. acquire iron which is very low in blood), Disseminate (between cells (being mobile)/between hosts (air-borne, faeces)), Cause disease (produce toxins).

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10
Q

Two ways bacteria colonise host? 3 ways intracellular pathogen survives?

A

Extracellular replicates outside cell. Intracellular replicates inside cell. [Links with adaptations] Access cell in phagosome (1) Escape phagosome (2) Prevent fusion with lysosomes (3) Survive in phagolysosome

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11
Q

Method of getting into cells – in the case of Salmonella?

A

Flagella propels bacterium to cell. Injectisome makes translocase complex (hollow pore) in membrane – pump virulence (harmful) proteins across its own membrane and that of host cell. Proteins interfere with actin proteins, causing actin polymerisation  membrane ruffling and bacterial internalisation. Allows to invade cells which are not naturally phagocytic.

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12
Q

Recap of previous Q: what are the 2 main functions of injectisomes pathogenically?

A

Pump pathogenic proteins into cell – contributes to virulence. Manipulates actin for entry into cell.

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13
Q

Method of manipulating actin – in the case of Listeria?

A

On tip of bacterium, actin polymerisation triggered which provides propulsive force for bacteria to move inside and between cells (they can propel themselves across membrane by pushing membrane of host cell against membrane of another cell  so cell membrane of host cell and the bacterium engulfed into invaded cell).

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14
Q

How do bacteria replicate? What is this type of DNA transmission called?

A

Binary fission. Vertical transmission of DNA. Means daughter cells identical parent.

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15
Q

How does variation occur vertically?

A

Mutation

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16
Q

3 mechanisms bacteria can exchange DNA?

A

Transformation Conjugation Transduction Horizontal transmission of DNA.

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17
Q

What is transformation?

A

DNA uptake Suck up DNA from extracellular space and integrate into its own. Single stranded DNA segment (naked DNA).

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18
Q

What is conjugative transfer?

A

Transfer from one cell directly to another across a mating bridge. In the form of a plasmid (circular, self-replicating DNA). Plasmid is replicated as it passes across bridge, so plasmid retained in original cell, and injected into other.

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19
Q

What is phage transduction?

A

Phage (short for bacteriophage – a virus that parasitizes a bacterium) replicates its DNA in bacterium and cuts bacterial DNA into small pieces. The short DNAs are packaged into phage heads – of which some bacterial DNA is picked up. Bacterium lyses and phages released. Phage injects obtained bacterial DNA into new bacterial cell – injected DNA may be incorporated into bacterial chromosome.

20
Q

What is purpose of horizontal DNA transfer?

A

Bacteria gain accessory genes which drives evolution – brings variation. Contributes to virulence.

21
Q

How do accessory proteins contribute to virulence?

A

Import pathogenicity islands – chunks of DNA that contribute to virulence e.g. producing a toxin, making an injectosome.

22
Q

What is virulence?

A

The severity or harmfulness of a disease

23
Q

What is infectivity?

A

Ability of an agent to infect. The characteristic of a disease agent that embodies capability of entering, surviving in, and multiplying and causing disease in a susceptible host.

24
Q

Possible sources of bacterial infection: two types?

A

Intrinsic – bacteria inside us.
Extrinsic – outside.

25
Intrinsic sources of infection?
Stomach and small intestine generally quite clean because of acidic properties of stomach. Don't cause disease because immune system coping. See image attached.
26
Extrinsic sources of infection?
Expected and unexpected sources. Expected: normal microbiota entering via an expected route. Unexpected: normal microbiota entering unusual site OR pathogenic microbiota entering any site. e.g. newborn baby in contact with maternal microbiota in birth (expected), and normal microbiota contact with baby via cut in skin (unexpected).
27
Portal of entry: upper respiratory tract – how are bacterial infections acquired?
Extrinsically acquired from droplets or airborne, hand transmission can act as an intermediate, mouth-to-mouth, hand-to-mouth.
28
What are the disease consequences of bacterial pathogens acquired via the upper respiratory tract?
All that needs to be learnt are places. e.g. sinusitis can spread to brain or ears. Upper respiratory tract can also spread down and to bloodstream. All the infections in bloodstream, and even pneumonia and abscess can lead to SEPSIS.
29
Portal of entry: urogenital tract – how are bacterial infections acquired?
Intrinsic sources – From large intestine bacteria. Urinary system: one hole into the urinary system that is close to large intestine exit. Genital system: same thing. Extrinsic sources – Urinary system: catheter insertion into bladder. Genital system: sexually transmitted.
30
Why do females have higher bladder infection incidence?
There’s one hole into the urinary system (urethra) that is close to large intestine exit. Distance shorter in women. Bacteria can pass between the two – intrinsic source.
31
What are the disease consequences of bacterial pathogens acquired via the urogenital tract?
Limited to bladder = cystitis. Travels upwards to kidneys = pyelonephritis. For both, most common = E. coli. Genital tract infections can also travel – up to Fallopian tubes in women. Can also have pregnancy complications where baby acquires natural microbiota from mother’s genital tract in delivery.
32
Portal of entry: broken skin – types of acquisition?
DON’T REALLY NEED TO MEMORISE, BECAUSE SHOULD BE QUITE EASY TO DETERMINE BY SELF – PLUS, MCD EXAM IS SHORT-ANSWER AND MULTIPLE CHOICE. Surgical wound, skin disease inc. eczema, drug using injections, insect bites leave broken skin = bacterial entry points (insect doesn’t necessarily give infection – can be through scratching…), cannular, animal bites.
33
Common bacteria in skin infections from broken skin? And complication from treatment?
S. Aureus. If patient has had a lot of antibiotics and in hospital = could mean MRSA.
34
What are the disease consequences of bacterial pathogens acquired via broken skin?
Bacteria could get under skin = cellulitis (deeper skin layers). Can cause abscess. Could infect connective tissue below skin without skin being involved at all. All could lead to blood infection.
35
Portal of entry: gastro-intestinal tract – how are bacterial infections acquired?
Contaminated food, water.
36
What are commensals?
Bacteria that don’t cause disease.
37
What is pathogenicity?
Ability to cause disease.
38
What are the factors affecting pathogenicity? And what do each of these factors depend on?
Infectivity and Virulence. Infectivity – ability to cause infection. Affected by: route of transmission (e.g. withstand stomach acid if gastro), ability to colonise, have tropism and motility, replicate, evade body’s immune system. [CPR Washington DC]. Virulence – features that enhance disease causation. E.g. toxin production, enzymes that degrade host molecules, interruption of normal host functions, immune evasion e.g. neutrophil death.
39
What is infectious dose?
Number of bacteria required to initiate infection.
40
What is sepsis and how does it happen? Causes?
Organ dysfunction because of infection. Sepsis is characterized by immune system response to infection that leads to tissue and organ damage. Excessive inflammation may be followed by decreased functioning of the immune system. Causes: too much pathogen virulence, not enough ‘good’ innate immunity to pick up pathogen when low levels.
41
Treatment for sepsis? (x4)
Antibiotics Intravenous fluids for dehydration, stop kidney failure and increase BP. Drugs to maintain BP. May have a lot of acid in their blood. Treated with oxygen.
42
What factors affect an individual’s infection susceptibility?
Age Stress levels Nutrition Immuno-sufficiency (drugs, HIV) Pre-existing diseases. Genetics.
43
What is Systemic Inflammatory Response Syndrome?
Response to infectious or non-infectious cause. Associated with cytokine release which results in widespread inflammation. Leads to Sepsis which leads to Septic Shock (severe sepsis).
44
Difference between sepsis and septic shock?
Sepsis = body’s reaction to an infection damages its own tissues and organs. Septic shock = after infection. Blood pressure drops à multiple organ failure.
45
[**Bacterial pathogens: list examples of important bacterial pathogens,** **explain how they are transmitted by different routes, a****nd the ways in which they cause disease**](https://medicine.sofia.imperial.ac.uk/map/mbbs-medicine/2018/4f652f93-f01c-443f-aed4-a7ebd85f77e1)
Mouth (droplet transmission): * *Tonsillitis:** _Streptococcus pyogenes._ * *Meningococcal septicaemia:** _Neisseria meningitidis_ colonises nasopharynx asymptomatically before invading epithelial then endothelial cells. Upper to lower respiratory tract and beyond: * *Pneumonia:** Strep pneumoniae. * *Nasal sinuses and into brain, orbit:** _Streptococcus pneumoniae_, _Streptococcus milleri_, _Haemophilus influenzae._ Faeco-oral transmission: **Cholera:** _Vibrio cholerae_. Ureo-genital transmission: **Infections in neonates: meningitis, septicaemia:** group B _Streptococcus_ from GI tract. Skin: _Staphylococcus aureus_
46
Support procedures during organ failure; AND,[Therapeutic targets: identify pathways and targets for treatment of infection...](https://medicine.sofia.imperial.ac.uk/map/mbbs-medicine/2018/16a9c7f0-11b1-40e2-bede-dbb8a5bc30f8)
...not in notes, but I don't think it matters anyway.