Respiratory Pathogens 1 Flashcards Preview

Microbiology 2 > Respiratory Pathogens 1 > Flashcards

Flashcards in Respiratory Pathogens 1 Deck (50)
Loading flashcards...
1
Q

what is he degree of pathogenicity of a disease determined y

A

proteins it expresses and how effectively it cn integrate enviro info

2
Q

what are some virulence mechanisms

A

bac adhesion
bac invasion
bac evsion host defnece
bac toxins

3
Q

what is the cycle of bac infectivity

A
entry 
attachment
multiplication
evasion of host defences
cause damage
release
spread
4
Q

what are the components of bc adhesion

A

structure ligand
surface mol
receptors

5
Q

what are some imp structure ligands

A

capsule (s progenies)
fimbriae (B pertusis)
cell wall (s aureus)
fibrils (s snguinis)

6
Q

what are some imp surface mols receptors

A
keratinocytes 
laryngeal epi cells 
epi cells
platelets
salivary proteins
7
Q

what can bac adhesion be

A

superificl/sytemic (metastasis)
extra or intracellular
access via general contact or injection

8
Q

what are some examples of invasion

A

organism erodes tooth
organsim persisks in epi
org injected via arthropod

9
Q

what are some common bac assc with caries and perio disease

A

caries - s mutans

peio - p gingivalis

10
Q

lames disease from

A

borrelia burghdorferi

11
Q

what does penetration of epithelium lead to

A

blood vessel end = blood circ
to phagocytic cells = both
lymphatic tissue end = accumulates in lymph nodes

12
Q

what are some ways a bacteria can evade host defences

A
immunity at mucosal surfaces 
destroy immune cells 
interfere with inflam response
evade innate immunity 
overcome acquires immune response
13
Q

how can a bacteria have immunity at mucosal surfaces

A

production of glycosidases and Sialidases
(s cocci and veillonlela)
proteases
binding proteins

14
Q

why is glycosylation of bac imp

A

imp for structure and function and resit to proteases

15
Q

why is silica acid on IgA imp

A

imp for immunoglobulin function

16
Q

what do proteases do

A

cleave hinge region of IgA normally protected by glycosylation
(s sanguines)

17
Q

what do the binding proteins assc with mucosal surface immunity do

A

M family proteins
bind Fc region of iG
(s pyogeens and s aureus)

18
Q

how does a bac interfere with cytokines

A

bac induce septic an ixic shock
TNF a, interferon and interleukins
myeloid, lymphoid and vasc respond to infection

19
Q

what are cytokines

A

group of regulatory proteins key to immune response

20
Q

what are endotoxins

A

gm -ve cell wall

LPS outer mem complex

21
Q

what are LPS components

A

toxicity - lipid A

immunogenicity - polysacc

22
Q

what does endotoxins induce

A

variety of inappropriate inflam responses that impair hosts response to pathogen

23
Q

what does he outer mem of gm -ve bac consist of

A
assymetirc mem 
LPS
peptidoglycan
lipoproteins
bind to receps on macrophages, b cells and other cells = cytokines
24
Q

what is SIRS

A

systemic Inflammatory Response Syndrome

25
Q

what are the ways of inflam cytokines being released

A

macrophages activated by LPS/endotixn or peptidoglycan

or

t cells activated by exotoxins

26
Q

how is complement evaded

A

capsules

  • prevent activation of C3 and C3B
  • mask bound C3b
27
Q

how is there evasion of phagocytic killing

A

PVL - s aureus
intracellular survival – M TB
type 3 secretion systems

28
Q

how is acquired immune repossess overcome

A

phase variation and antigenic variation

29
Q

what is phase variation

A

switch between on and off forms of a gene
flagellin gene of salmonella
opacity genes of neisseria

30
Q

what is antigenic variation

A

allows bac to change sequence of a gene

pilin genes of neisseira

31
Q

what are the early symptoms of diphtheria

A

sore throat, low fever, swollen neck glands

32
Q

what are the late stages of diphtheria

A

airway obstruction
breathing difficulty
shock

33
Q

what are outbreaks of diphtheria assc with

A

unsanitary conditions
immunity gaps
vaccination fail

34
Q

what is the product of diphtheria

A

toxin = acute inflammation and formation of pseudomembrane

  • dead tissue
  • fibrin
  • polymorphs
35
Q

what causes diphtheria

A

corynebacterium diphtheria

  • gm +ve bacilli
  • aerobic non motile
  • toxin prod
36
Q

how is diphtheria transmitted

A

direct contact droplets/skin, or indirect via contaminated object

37
Q

explain some characteristics of corynebacterium diphtheria

A
sol 3 domain P's 
endocytosed
proteolytic cleavage 
catalytic domain 
translocate domain
38
Q

what is the treatment of diphtheria

A

inoculation with antitoxin

penicillin or erythromycin to slim bac

39
Q

how is diphtheria prevented

A

active immunisation
diphtheria formal toxin
booster and multiple vaccine

40
Q

what is whooping cough

A

highly contagious

life threatening

41
Q

what causes whooping cough

A

bordetella pertussis

gm -ve cocci

42
Q

what are the symptoms of whooping cough

A
severe cough 
low/no fever at start
choking 
nocturnal coughing
short breath
vomit
43
Q

how does bordetella pertussis enter

A

via resp tract
attach to ciliated epi
mediated by filamentous hem agglutinin
pert actin

44
Q

what is pertactin

A

outer mem protein

promotes attach to tracheal epi cells

45
Q

what are the toxins assc with bordetetlla pertussis

A

pertussis toxin
adenylate cyclase
tracheal cytotoxin

46
Q

what does tracheal cytotoxin do

A

kills ciliated cells and stimulates their extrusion from the mucosa

47
Q

what is pathogenesis

A

growth on ciliate epi and toxin prod

  • paralyse cilia tracheal cytotoxin
  • stim inflam resp
  • kill leucocytes
48
Q

what does pertussis toxin do

A

disrupts cell function
increases mucus secretion
incapacitates phagocytes

49
Q

what is the diagnosis and treatment of whooping cough

A
cough plate 
swab pharyngeal walls
erythromycin 
remove mucus
Ab therapy for secondary infections
50
Q

how is whooping cough vaccinate

A

part of multiple vaccine
kill b pertussis
3 antigenic types