methods of pathogenicity Flashcards

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1
Q

describe interferon

A

virus invades cell
host cell produces interferon
molecule of interferon will go to second cell
second cell begins producing antiviral proteins
AVP block viral replication

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2
Q

name the 4 types of adhesion molecules

A
  • fimbrae
  • capsule/slimelayer
  • protein spikes
  • flagella
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3
Q

name two types of toxins and who produces them

A

endotoxin - by gram negative only

exotoxin - produced by both gram negative and positive

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4
Q

describe a gram positive cell wall

A

circles
line
PEPTIOGLYCAN
CYTOPLASMIC MEMBRANE

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5
Q

describe gram negative cell wall

A

endotoxin (liposaccaride)
fuzzy lines
PEPTIOGLYCAN
fuzzy lines

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6
Q

name 4 cell associated virulence factors of S.aureus

A

capsule
protein A – fimbrae
fibronectin – binding protein
collagen binding protein

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7
Q

name virulence factors of s.aureus

A
enterotoxins
epidermolytic toxin
TSS toxin
membrane damaging toxin (haemolysins)
leucocidin
staphlokinase
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8
Q

describe HIV

A

immunosuppression
long lasting depression of humeral antibodies and CMI
antigenic variation
variation between individuals
variations within same patient
unto 108 genetic variants of HIV in AID patients

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9
Q

describe gene switching

A

most dramatic form of antigenic variation
WHOLE sequence of genes coding for surface antigens switched on or off
e.g
TRYPANOSOME (sleeping sickness) has approx 1000 distinct surface molecules
organism can switch from one gene to another at roughly weekly intervalls

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10
Q

describe antigenic shift

A

major changes in surface antigens caused by recombination between virus strains

e.g human influenza A strain and avian flu virus –» new strain of influenza –> influenza pandemic

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11
Q

describe antigenic drift

A

small mutations in gene coding for surface antigens
reduces effectiveness of B&T cells memory built up in response to earlier infection
e.g all types of common cold or influenza

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12
Q

describe antigenic variation

A

variation in surface antigen composition
various forms:

antigenic shift
antigenic drift
gene switching

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13
Q

describe inflamation

A

dilation of blood vessels in infected area causes
FIBRONECTIN and white blood cells to arrive at infection site
protein rich fluid to be secreted
fibrin seals blood vessels leading from infection site
macrophages and neutrophils move towards site by chemotaxis

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14
Q

describe NON specific defences of the CONJUNCTIVA

A

main defence = keep blinking
tears contain lysozyme
only need slight damage to allow organisms such as chlamydia to cause infection

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15
Q

describe NON specific defences in UROGENITAL TRACT

A

bladder has no normal flora
flushing action removes organisms

VAGINA– normal microflora protects against pathogens but disturbance to normal flora can lead to thrush

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16
Q

describe NON specific defences in ORAL CAVITY

A

flushing action of saliva (approx one litre per day)
lysozyme and antibodies in saliva
normal microflora
influence of diet– e.g. vitamin C deficiency

17
Q

describe NON specific defences in GI TRACT

A
constant digestive flow
removes microorganisms
acidic PH
bile salts
digestive enzymes
mucous lining gut epithelium
large population of resident bacteria
competition some produce inhibitory substances
18
Q

name 3 infections that can attack healthy skin

A

ring worm
HPV
athletes foot

19
Q

describe NON specific defence SWEAT GLANDS

A

flush microbes from the skin

lysozyme

20
Q

describe NON specific defence SEBUM

A

oil substance from salacious glands

contains fatty acids

21
Q

describe NON specific defence SKIN

A
dry, tough, salty layer PH 3-5 (ACIDIC)
normal  microflora
desquamation -- skin cells shed at rate 5X10 to power8 per day
healthy intact skin rarely penetrated 
need damage of some kind
22
Q

absence of suitable target for immune responce… describe

A

weakly immunogenic capsular antigens mask more immunogenic cell wall compounds
organisms avoid immune forces by staying inside infected cell (leprocy)
mimicry of host antigens
e.g B-heamolytic streptococci and human heart muscle – rheumatoid heart disease

23
Q

name microbial strategies to overcome immune responce

A

resistance to phagocytosis
immunosuppression
absence of suitable target for immune resource e.g possession of capsule

24
Q

name two types of defences the body has against infection

A

NON SPECIFIC (inane)

SPECIFIC (adaptive)

25
Q

name and describe RT pathogens

A

bordetella pertussis – produces toxin that paralysis cilla

influenza virus –

both have HAMAGGLUTININS on their surface attach strongly to receptor sites on lining on upper RT

26
Q

name infections caused by S.aureus

A

boils, skin septic, post operative wound infections, scaled skin syndrome, catheter associated infections

septicaemia, endocarditis, TSS, ostoeomyrlitis, phnemonia, food borne infections

27
Q

describe the mechanism of resistance to phagocytosis

A

capsule prevents contact with phagocyte
prevention of ozonisation
escape into cytoplasm
phagocyte destroyed by release of toxin

28
Q

describe the flow chart when the infection is not contained

A

spread by lymphatics – antibody formed bacteria killed

toxin produced – antibody formed, toxin neutralised,

intracellular multiplication – cell mediated immunity

ALL INFECTIONS CONTAINED BY IMMUNE RESPONCE

29
Q

MICRORGANISMS

INATE DEFENCES – entry prevented no infection
(mechanical barriers, secretions, mechanical elimination, phagocytic cells)

INVASION
local multiplication

INFLAMATION – infection contained

A

MICRORGANISMS

INATE DEFENCES – entry prevented no infection
(mechanical barriers, secretions, mechanical elimination, phagocytic cells)

INVASION
local multiplication

INFLAMATION – infection contained