W3 13 Intro To Microbial World Flashcards

1
Q

What can cause infection?

A

Bacteria, viruses, fungi, parasites, Protozoa, helminths

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2
Q

What is a parasite?

A

Organisms that live on/in another host and derive nutrition without benefit to the host

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3
Q

What are helminth?

A

Worms, parasitic eg tapeworms

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4
Q

What are Protozoa?

A

Single cells eukaryotic cells. Many types, can be parasites. Can be visible with naked eye.

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5
Q

What is a major insect borne parasite?

A

Plasmodium - cause of malaria, transmitted by mosquitos

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6
Q

Examples of food borne parasites

A

Giardia, cryptosporidium, Taenia

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7
Q

Describe the differences between prokaryotes and eukaryotes

A

Eukaryotes - DNA in nucleus, DNA has histones, organelles are membrane-enclosed, cell walls of present are chemically simple, cell division by mitosis
Prokaryotes - DNA not enclosed by a membrane, lacks membrane-enclosed organelles, cell walls made from peptidoglycan, divide by binary fission

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8
Q

Are bacteria or viruses bigger?

A

Bacteria are wayyyyyyy bigger

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9
Q

How can you classify bacteria?

A

Via gram stain
Morphology
Oxygen requirments

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10
Q

Describe the difference in cell walls of gram positive and gram negative bacteria

A

Gram positive - many layers of peptidoglycan = thick cell wall. No outer membrane
Gram negative - thin peptidoglycan layer embedded between an inner and outer membrane

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11
Q

How does dye distinguish from gram positive and gram negative?

A

Blue or purple dye from crystal violate penetrates the many peptidoglycan layers of gram positive bacteria and is held within these layers. In gram negatives, the stain is washed away by a decolorisation step. The counter stain which is pink or red will colourise those bacteria.
Positive = blue/purple
Negative = red

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12
Q

Give examples of gram positive bacteria

A

Staphylococci
Streptococci
Lactobacilli
Clostridia

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13
Q

Give some examples of gram negative bacteria

A

Enterobacteriaceae
P gingivalis
F nucleatum

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14
Q

Stages for the diagnosis of infectious disease

A

Symptomatic patient —> clinical examination —> presumptive clinical diagnosis —> tests selected by primary care clinician —> sample/specimen collection —> lab tests —> definitive diagnosis —> drug tests —> treatment/therapy —> asymptomatic patient

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15
Q

What different diagnostic laboratory tests are there?

A

Direct examination/microscopy —> stain
Culture —> biochemical analysis; toxin testing
Antibody detection methods —> agglutination; rapid test; ELISA
Genetic —> hybridisation; PCR; RT-PCR

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16
Q

How can viruses be detected via serology?

A
  • detection of virus particles
  • detection of viral antigens
  • anti-viral antibody detection
  • viral nucleic acid detection
  • cytological or histological examination of cells from site of infection
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17
Q

What is ELISA?

A

Used to detect viruses and bacterial cell surface antigens or toxins
May be qualitative or quantitative - blood sample tested

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18
Q

Describe some characteristics of fungi

A

Eukaryotic, single or multicellular, cell wall contains chitin

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19
Q

What fungi causes oral thrush/candidiasis?

A

Candida (albicans) infects the mucosal membranes of the mouth

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20
Q

When is oral thrush common?

A

In immunodeficiency patients (and risk factor for systemic spread)
Requires anti fungal treatment

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21
Q

Where is Cryptococcus neoformans (yeast) clinical seen?

A

Meningitis in HIV, cancer patients, pulmonary disease like pneumonia
Can have oral manifestations

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22
Q

What is the predisposition for the manifestation of cryptococcus neoformans?

A

Defects in cell-mediated immunity (low CD4+ T cells)

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23
Q

Where is cryptococcus neoformans found?

A

Environmental organism: soil, bird droppings
It is an important opportunistic pathogen

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24
Q

What is aspergillus fumigatus?

A

Filamentous fungus found in ubiquitous spores - soil, dust (building work etc)

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25
Q

What clinical illnesses can aspergillus fumigatus cause?

A

Sinusitis, endocarditis (post valve surgery)
Pulmonary: asthma etc
Systemic: lung, renal, cerebral (in immunocompromised)

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26
Q

Treatment for aspergillus fumigatus

A

IV voriconasole or Amphoteracin B (Liposomal)

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27
Q

Properties of viruses

A

Do not grow or divide independently
Are obligate intracellular parasites
Contain DNA or RNA (never both)
Unable to generate ATP
Unable to synthesis proteins independently
Are acellular (and not bound by a cytoplasmic membrane)

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28
Q

What is the structure of a virus

A

Not bound by a cytoplasmic membrane
Often possess a proteinaceous capsid which surrounds the nucleic acid (nucleocaspid)
In some cases viruses are surrounded by a lipid membrane envelope derived from the host

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29
Q

How are viruses classified?

A

Baltimore classification system based on their replication strategy

30
Q

What is the life cycle of a virus (common features as can vary greatly)?

A

Attachment to host cell
Entry of host cell
Loss of envelope/release of viral nucleic acid
Replication of genome and protein production
Assembly of new viruses
Release from cell - escape to infect new host cells

31
Q

Give 2 examples of where viruses affect oral health

A

Herpes simplex - infects healthy individuals, causing sores/blisters in mouth
Human papilloma virus and cancer - carriage of HPV is a strong risk factor for oropharyngeal cancer in patients with dental disease

32
Q

What is plaque?

A

A bacterial biofilm - a community of bacterial attached to a surface and encased in a polysaccharide matrix

33
Q

What is resident flora?

A

Consists of relatively fixed types of microorganisms regularly found in a given area at a given age. Promptly reestablishes itself if disturbed. Acquired rapidly during and after birth. Reflects age of a person. Changes continuously throughout life. Reflects nutrition, genetics, environment and sex of a person.

34
Q

What is transient flora?

A

Consists of non-pathogenic or potentially pathogenic microorganisms that inhabit the skin or mucous membranes for hours, or days.

35
Q

Give some symbiotic relationships of microbe and host and what they mean

A

Mutualistic - both organisms benefit - ‘mutually beneficial’
Commensalistic - one organism benefits, the other is neither helped nor harmed
Opportunistic - under normal conditions, microbe does not cause disease, but if conditions become conductive, it can cause disease
Pathogenic (parasitic)
Dysbiosis

36
Q

What happens to a dental biofilm in health?

A

Symbiosis and balanced equilibrium between microbe and hosts and factors like diet, lifestyle, hormones, hygiene, host defences

37
Q

Where can pathogens be acquired from?

A

Food, drinking water, soil/environment, hospital acquired, other humans

38
Q

What can cause a dysbiosis of the oral health?

A

Inappropriate diet
Inadequate plaque control
Impaired saliva flow
Altered host defences
Lifestyle risk factors
Microbe-microbe interactions actions get altered

Lead to caries and periodontal diseases!

39
Q

What bacteria are present in caries?

A

Acidogenic - mutans streptococci; lactobacilli

40
Q

What bacteria are present in periodontal diseases?

A

Spirochaetes, P gingivalis, T forsythia, A.A.

41
Q

What are the steps in infection from pathogenic mechanisms?

A

Attachment/entry - colonisation
Multiplication (and dissemination) within the host
Evasion of host defences
Damage to the host
Transmission to new host

42
Q

Sites of colonisation of pathogens

A

Skin
GI tracts
Conjunctiva
Respiratory tract
Urinary tract
Oral cavity

43
Q

How do pathogens multiply/disseminate?

A

Direct spread - confined to local environment; extension to neighbouring tissues
Presence of fluid movement - eg lungs instestines, urinary tract

44
Q

How can bacteria be spread through body?

A

Via blood - effective means of spread, resistant to Antimicrobial factors, invades cells, bacteraemia
Via lymphatic networks - reach lymph nodes, can grow in lymphatic endothelium
Via CSF - enter from the blood
Via pleural and peritoneal cavity

45
Q

What antigenic variation is there between microbes?

A

Surface structure may be antigenic - elicit an immune response —> killing
Changing surface structures —> immune system cannot recognise bacteria (by changing antigen on surface)

46
Q

How can microbes destroy immune system components?

A

IgA1 proteases
Complement degradation
Complement inhibition
Destruction and inhibition of cytokines

47
Q

What pathogenic mechanisms to cause damage are there? (Images pg142)

A

Endotoxins
Exotoxins
Enzymatic lysis
Pore formation
Inhibition of protein synthesis - produces a toxin which enters cells
Hyper activation - opens too many channels so loses ions, causing dehydration
Effects of nerve-muscle transmission - leads to flaccid paralysis

48
Q

How can pathogens transmit to a new host?

A

Horizontal spread - infected air, water, food, contact, vectors etc
Vertical spread - hereditary passing onto offspring

49
Q

What are antibiotics?

A

A variety of substances derived from microorganisms that control the growth of or kill bacteria

50
Q

What is AMR?

A

Antimicrobial resistance

51
Q

Why is AMR a concern?

A

Won’t be able to treat someone if they have been infected by a resistant strsin

52
Q

Why is AMR developed?

A

Antibiotics fed to livestock, get into soil, plants, water systems and us.
Used by hospitals, prescribed by GPS, and by humans transmitted to environment
So bacteria have more opportunity to become resistant

53
Q

What is the method for agar diffusion assay 1?

A

Take bacteria you want to test and spread thinly onto agar plate
Place antibiotic discs onto it
Incubate overnight, at 37°C
Examine plates for zones of inhibition

54
Q

What do you expect to see as the results from agar diffusion assay 1?

A

Opaque yellow colour = bacteria growing
Discs with a halo = zone of inhibition
Clear area is where bacteria have not been able to grow since antibiotic diffuses out into the agar, and halts certain bacterial growth

55
Q

What is different about agar diffusion assay II - semi-automated?

A

Addition of the discs is automated. Same agar plate and bacteria etc.

56
Q

When would you use agar diffusion assay III with E (ellipsometer) test?

A

If you want to know the exact concentration that will kill the bacteria

57
Q

How is an E test for MIC different? (Pg146)

A

Strip instead of a disc is impregnated with antibiotic at different concentrations
During incubation, the antibiotic diffuses out and sets up a gradient

58
Q

How are the results from an E test different and how are they interpreted?

A

Zone of inhibition is an elliptical shape, because concentration of antibiotic at top of E strip is highest and gets lower and lower, so at top there is no growth at all
At some point you see a meniscus, which is the lowest concentration that we can use to inhibit the bacteria = minimum inhibitory concentration MIC, important for deciding dosages

59
Q

Are broth dilution assays better than agar diffusion assays?

A

They are more accurate, but more involved so not as practical
Quantitative rather than qualitative
Can determine the MIC

60
Q

What is the method for a broth dilution assay? (Pg146 image)

A

Need a whole range of tubes containing broth so bacteria can grow in it and a dilution series of the antibiotic
Then inoculate (add bacteria to) the tubes
Incubate overnight

61
Q

Results from a broth dilution assay

A

Then see which tubes have growth. At the concentration where bacteria have not managed to grow is the MIC

62
Q

Antibiotics can either kill bacteria or haunt their growth. How do we find out which one it can do?

A

Using an agar plate, plate each tube, a small proportion onto the plate
Incubate overnight

63
Q

What would the results be if the antibiotic is bacteriocidal?

A

No bacteria would grow on the plates above the MIC concentration, but would grow on the plates that bacteria already grew in the broth.
Some but less bacteria might grow on the MIC plate, since the minimum bacteriocidal concentration MBC is sometimes higher than the MIC.

64
Q

What would the results be if the antibiotic was bacteriostatic?

A

There would be bacteria growth on every plate, because the growth is only halted, the bacteria have not been killed. (Plates have no antibiotic on them so can grow again)

65
Q

What are the classes of antibiotics?

A

Broad-spectrum
Bacteriostatic/bactericidal

66
Q

What does broad-spectrum mean?

A

Antibiotics can work against many different bacteria

67
Q

Which antibiotics are just bactericidal?

A

Penicillin G - well on gram pos
Ampicillin - well on gram pos and some neg
Amoxicillin - well on pos and some neg
(All these inhibit bacterial cell-wall synthesis)

68
Q

What antibiotics are bactericidal and bacteriostatic?

A

Gentamicin - mainly against gram neg. Depends on dose and what bacteria you use it against whether it is cidal or static. Binds to ribosomes.

69
Q

Examples of bacteriostatic antibiotics

A

Tetracycline - binds to ribosomes - well against gram neg and positive - broad-spectrum
Chloramphenicol - inhibits protein synthesis

70
Q

Where can antibiotics target?

A

Cell-wall synthesis
Cell membranes
Protein synthesis
Nucleic acid synthesis

71
Q

What is the MIC?

A

The lowest dose of an antimicrobial agent that is required to inhibit growth