microbiology 227 Flashcards

1
Q

gram staining

A

Done with crystal violet stain

Gram positive retain the violet dye

A counterstain is added (commonly safranin or fuchsine) and this will wash off the crystal violet from those bacteria which haven’t retained the stain i.e Gram negative

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2
Q

gram +ve

A

tend have a single membrane (monoderm) surrounded by a thick peptidoglycan

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3
Q

gram -ve

A

posses a thin layer of peptidoglycan between 2 membranes (diderms)

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4
Q

bacterial morphology options

A
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5
Q

5 stages in bacterial biofilm growth

A
  1. Reversible attachment of planktonic cells
  2. First colonisers become irreversibly attached
  3. Growth and cell division
  4. Production of EPS (exopolysaccharides) and formation of water/nutrient channels
  5. Attachment of secondary colonisers and dispersion of microbes into new sites
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6
Q

caries progression

A

S.Mutans is exposed to sucrose in the oral cavity and metabolises it producing two things

  • Lactic Acid - that demineralises the tooth tissue
  • Glucans - these allow adhesion of S.Mutans to other organism
    • Soluble (water) glucans
    • Insoluble glucans

The pH of the environment decreases to more acidic, but the bacteria, gain ATPase pumps to put out H+ ions to gain acid tolerance

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7
Q

streptococci and acid production

A

In normal ph they use the Phosphotransferase system to uptake sugars

In low ph environments they can utilise a lower affinity transport system to take up sugars to survive

  • which if they didn’t have it would mean they would starve

They do this by taking advantage of the ph gradient

ICF – high ph , ECF – low ph

use this to uptake sugar

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8
Q

key organisms in caries

A
  • sterptococcus mutans
  • streptococcus spp
  • lactobacillus acidophilus
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9
Q

key organisms in periodontal disease

A
  • pophymonas gingivalis
  • treponema denticola
  • prevotella intermedia
  • agrregnacter actinomycetemcomitans
  • fusobacterium nucleatum
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10
Q

key organisms in endo infections

A

porphyromonas endodontalis

prevotella intermedia

enterococcus faecalis

fusobacterium nucleatum

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11
Q

key organisms in candiasis

A

candida albicans

candida glabrata

candida tropicalis

staphylococcus aureaus (in angular chelitis)

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12
Q

Newtown’s type 1 inflammation

A

localised

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13
Q

Newton’s type II inflammation

A

diffuse

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14
Q

Newton’s type III inflammation

A

granular

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15
Q

4 bacterial resistance mechanisms

A
  1. blocking entry
  2. inacivating enzymes
  3. alteraion of target molecule - enzymes in the organism alter the receptor the antibiotic/fungal would previously bind to
  4. efflux of antiobiotic - efflux pumps
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16
Q

fluoride 2 actions

A

remineralises enamel

inhibits ATPase’s ability to produce hydrogen ions

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17
Q

supragingival plaque predominately

A

aerobic bacteria

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18
Q

subgingival plaque predominately

A

anaerobic bacteria

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19
Q

p gingivalis properties

A

has pilli that allow it to co-aggregate with other bacteria

produce gingipains can degarde chemokines

inc MMPs - cause dysbiosis (unbalanced mucrobial community)

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20
Q

Periostat

A

doxycycline - inhibits MMPs

reduces immune inflammatory response

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21
Q

denture stomatitis is only

A

pseudomembranous

not tissue invasion

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22
Q

c albicans or glabrata more resistant to azoles

A

c glabrate

if see hyphae in scraping more likely albicans

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23
Q

azoles are

A

fungostatic

need mechanical action to kill of bacteria

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24
Q

denture stomatitis caused by

A

plaque biofilm

non specific

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25
Q

what can occur if abscess left untreated

A

endotoxic shock or super-antigen infection

incision and drain to take sample for anaerobes

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26
Q

potentially life threat of submandibular abscess

A

respiratoy compromise

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27
Q

habitat

A

site where organism grows

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28
Q

microbial community

A

MO growing in particular habitat

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29
Q

ecosystem

A

MO community in a specific habitat and their surroundings

  • Physical, Chemical and Biological properties dictate composition of community
  • Those which survive and dominate and those which die
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30
Q

niche

A
function of an organism within its community – organisms compete for a niche, in mixed communities it is only stable if there is
a niche for all the different types of organisms
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31
Q

resident microflora

A

organisms regularly isolated (found) in a site

32
Q

pathogens

A

MO with potential to cause disease

33
Q

oppurtunistic pathogens

A

organisms with the potential to cause disease

34
Q

dental plaque

A

Bacteria and degraded mammalian cells , surrounded by matrix containing both protein and polysaccharide

35
Q

saliva role in MO in mouth

A

Lubricates mouth
Buffering effect
Mucins and Glycoproteins (saliva components) do the following

  • Adsorb to tooth surface – create pellicle for mic-orgs to attach
  • Nutrient source for bacteria (Carbohydrate, Protein)
  • Aggregate mic-orgs and clear them from the mouth
  • Inhibit growth of some bacteria
36
Q

gingival crevicular fluid role in MO in mouth

A

Serum-like fluid
Nutrient source
Flow can remove non-adherent organisms
IgG, IgA, IgM, complement system

37
Q

factors affecting microbial growht in the mouth

7

A

temperature

anaerobiosis

pH

nutrients

adherence

antimicrobials

host defences

38
Q

pH and microbial growth

A

pH 6.5 in mouth ideal for microbial growth

pH 5.0 after sugar intake – lactate produced by bacteria, saliva can’t penetrate plaque at the enamel surface

pH gradient exists, in caries acid producers like Strep and Lactobacilii assume a larger niche = ph falls even lower

39
Q

factors in microbial adherence

A

EPS promotes adherence to surfaces

  • Adhesins (lectins, fimbrils, lipoteichoic acid)
  • Receptors (sialic acid on epithelial cells, collagen, fibronectin) – host derived factors
40
Q

colonisation

6 steps

A
  1. Obtain Nutrients from Saliva and diet
  2. Tolerate variables – ph, oxygen tension, ionic strength
  3. Overcome host defences
  4. Grow at rate either greater than or equal to other species
  5. Resist other bacteria that may prey on them or that produce toxins
  6. Adhere to surfaces
41
Q

gram +ve bacteria morphology

A

Cell wall

  • Thick multi layered
  • Cross linked Peptidoglycan
  • Teichoic and lipoteichoic acid
  • Retains crystal violet stain
42
Q

gram -ve bacteria morphology

A

Cell wall
- Doesn’t retain the gram stain

Outer membrane

  • Unique to gram –ve
  • Contains transmembrane proteins e.g porins
  • Allow diffusion of hydrophilic molecules through membrane

Periplasmic space

  • Between outer membrane and cytoplasmic membrane
  • Contains sugar transport systems
  • Hydrolytic enzymes (breakdown macromolecules for metabolism)
43
Q

2 types of passive transport

A

simple diffusion

facilitated diffusion

44
Q

simple diffusion

A

molecule moves directly through opening/pore in membrane without interacting with another molecule

  1. Through a lipid bilayer
  2. Through a membrane pore
  3. Through a channel in a protein cluster
45
Q

facilitated diffusion

A

Molecules transported across membrane by binding to one or more carrier protein in the membrane

  1. Single transport protein
  2. Delivery by several protein components
  3. Through a gated channel in a transmembrane protein

Transport molecules involved in Facilitated diffusion

  • Uniport – Single solute carrier from one side
  • Symport – Co-transport of two different substances in the same direction
  • Antiport – co-transport of two different substances in the opposite direction
46
Q

active transport

A

Energy required to move substances uphill against a concentration gradient

  • provided by ATP and a specific ATPase
47
Q

3 types of active transport

A

H+/lactose symporter

phophotransferase sysyem

histidine periplasmic system

48
Q

H+/lactose symporter

A

active transport

Ionic gradients/membrane potential provides energy

Co-transport of sugar/amino acid along ionic conc. Gradient

H+ translocation creates electrochemical gradient that drives uptake of lactose

49
Q

phosphotransferase system

A

active transport

Glucose phosphorylated into glucose-6-P > GLYCOLYSIS > PEP

Glucose + PEP -> Glucose-6-P + pyruvate

catalysed by an enzyme II complex

50
Q

histidine periplasmic system

A

active transport

Occurs between outer membrane (where histidine enters) and the cytoplasmic membrane

HisJ binding proteins wait in the periplasmic space

Histidine forms a complex with HisJ

Histidine-HisJ complex binds to membrane components

Intracellular ATP hydrolysed by the complex which allows Histidine to cross over into the inside of the bacteria

51
Q

EPS contains

A

mutans

dextrans/levans

52
Q

mutans in EPS

A

gel like - inc bulk of plaque

insoluble so create highly anaerobic conditions between plaque fluids and saliva

assist in bacterial attachment

53
Q

dextrans/levans in EPS

A

carbohydrate reserve

levan is rapidly metabolised and is degraded v quickly by oral bacteria

54
Q

carbohydrate production and acid production in aerobic conditions

A

outer surface of plaque

Pyruvate is completely oxidised to CO2 and H20 via Kreb’s cycle and respiratory chain

NADH formed in krebs cycle is oxidised by respiratory chain

55
Q

carbohydrate production and acid production in anaerobic conditions

A

inner surface of plaque

Pyruvate -> lactate

orther organic acids are formed - low pH in dense plaque

56
Q

Kaposi’s Sarcoma

A

Affects mucous membranes, skin and lymph nodes
Purple lesions

Associated with HHV-8 (Human Herpes Virus 8)

57
Q

HIV and AIDS

A

Acute primary infection
o Glandular fever like
o 10% symptomatic

Latent period
o Patient asymptomatic
o Can be latent 8-10 years

Symptomatic stage
o ARC (AIDS related complex)
o Hyperactive B-cell response
o Follicular/mixed hyperplasia of lymph nodes

Oral Lesions associated w/ HIV

  • Erythamatous Pseudomembranous Candidiasis
  • Hairy Leukoplakia
  • Kaposi’s sarcoma
  • Non-Hodgkin’s Lymphoma
  • Periodontal disease
    • Linear gingival erythema
    • Necrotising Ulcerative gingivitis
    • Necrotising Ulcerative periodontitis
  • Paediatric HIV – Parotid Enlargement
58
Q

bacteriostatic

A

inhibit proliferation of bacteria

59
Q

bacteriocidal

A

substance kills bacteria

60
Q

detergent

A

group of synthetic organic water soluble agents that contain the following
▪ wetting agents
▪ emulsifying agents
▪ soil holding properties

61
Q

disinfectant

A

process for the removal/destruction of microbes (not usually bacterial spores)

62
Q

staphylococcus aureus

desc

virulence factor

disease

A

DESCRIPTION

  • gram positive, occurs in clumps

VIRULENCE FACTOR

  • Panton-Valentine Leukocidin toxin > leads to tissue necrosis

DISEASE

  • Pyogenic infections – pus (boils, abcesses, wound infections)
  • Toxin mediated- Toxic shock syndrome
63
Q

streptococcus pyogens

desc

virulence factor

disease

A

DESCRIPTION

  • gram positive

VIRULENCE FACTOR

  • Super antigens, toxic shock syndrome

DISEASE

  • Acute Rheumatic fever, Glomerulonephritis, Meningtitis, pharyngitis, toxic shock
64
Q

streptococcus anginosus

desc

virulence factor

disease

A

DESCRIPTION - gram positive

VIRULENCE FACTOR - Intermedilysin

DISEASE- Bacteremia, Splenic Abcess

65
Q

clostridium perfingencs

desc

virulence factor

disease

A

➢ DESCRIPTION - Anaerobes
➢ VIRULENCE FACTOR - Alpha toxin (Lecinthinase)
➢ DISEASE - Myonecrosis, Haemolysis

66
Q

herpes simplex

desc

virulence factor

disease

A

DESCRIPTION - DNA envelope virus

VIRULENCE FACTOR - Causes cell lysis

DISEASE - Herpes labialis

67
Q

candida albicans

desc

virulence factor

disease

A

DESCRIPTION - Gram +ve fungi

VIRULENCE FACTOR- Phospholipase

DISEASE- Erythamatous Candidiasis, Pseudomembranous Candidiasis

68
Q

impetigo

A

epidermis infection

requires fibronectin to infect breaks in skin

caused by staph

69
Q

angular chelitis

A

epidermis infection

candida albicans or staph

70
Q

erysipelas

A

infection of dermis

rasied rosy rash

disappears on pressure

group A staph

71
Q

folliculitis

A

infection of hair follicles

staph

treated with antibacterial soad and antibiotics (cephalosporin, dicloxacillin)

72
Q

cellulitis

A

infection on subcutanous

non suppartive bacterial infection

group A staph

infection of connective tissue and interstitum and not cells themselves (misnomer)

73
Q

necrotising fascitis

A

infection of fascia

can result in septicaemia

gram +ve and -ve bacteria

74
Q

myonecrosis

A

clostridium perfringens

casues deep trauma with groww contamination

infection of muscle

75
Q

gangrene

A

wet type is bacterial

clostridium perfringens and bacillus fusiformis

infecition of muscle