extracellular infection Flashcards

1
Q
  • interstitial spaces , blood , lymph and works on epithelial surface for bacteria fungi protozoa and helminth —>
  • cytoplasmic for virus and works on vesticular for bacteria fungi protozoa
A
  • extracellular
  • intracellular
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2
Q

— bacteria/paarsites that live and mutably outside the body as:
➢ Streptococci pyogenes
➢ Staphlococcus aureus
➢ Haemophilus influenza ( its bacteria not a virus )
➢ Schistosoma mansoni
— orgasims that invade a cell to survive/mulibly/evade detection as:
vive/multiply/evade detection
➢ Listeria monocytogenes
➢ Mycobacterium tuberculosis
➢ Viruses (truly intracellular)

A

extracellular
intracellular

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3
Q

cooperation between innate and adaptive immunity is required:
—- and — at site of infection early line of defence in innate immunity
– and existing cculating – specific to outer coat proteins or lipids
- antigen presentation to T cells will activate —- and —-

A
  • macrophages and dendritic cells
  • b cells and antibodies
  • t helper and cytotoxic
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4
Q

innate immunity to extracellular infection actions in:

A
  • complement activation
  • phagocytosis
  • inflammatory response
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5
Q

complement activation :
—- pathway is activated by antibody recognition from previous infections
—- pathway is activated by peptidoglycans in cell walls of gram positive and gram negative bacteria
—- pathway is activated by bacteria that express mannose on their surface
—- formation is important for the neisseria species

A

classical
alternative
lectin
MAC
( check slides for graph plss)

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6
Q

phagocytosis is initiated by — and —-
killing of microbes happens in — via — and —
activation of innate immune cells cause production of —- as:

A
  • mannose receptors and complement receptors
  • phagolysome
  • reactive oxygen species ROS and nitric acid NO
  • inglammatory mediators as:
    ➢ TNF, IL-1, IL-6, IL-8, prostaglandin etc
    mediate inflammation
    ➢ Instructive cytokines to guide T cells differentiation
    ( check slide 11 for pic pls)
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7
Q

adaptive immunity to extracellular micorbes use:

A

helper T cells and antibody production for b cells
( check slide 12)

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8
Q

immune response to streptococci:
1- gram —- bacteria and is —
2- shaped —
3- its —
4- coat is rich in —
5- release —
6- includes:

A

positive
aerobic
spherical
encapsulated
polysaccharide rich coat
toxins
streptococcus pyogenes and streptococcus pneumonia

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9
Q

the most common medical injuries of streptococcus are:
the most serious are:

A

most common:
- pharyngitis
- skin infections as:
- impetigo
- scarlet fever
- cellulite
most serious:
- toxic shock syndrome
- penumonia
- necrotising fasciitis

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10
Q

the overview of immune response to steptococci:
- — microbe
- resident — indue phagocytosis and inflammation
- recruitment of —
- antigen presentation to —
- —- production by —

A
  • extraceullar
  • macrophages
  • neutrophils
  • CD4+ t helper cells
  • antibody production by b cells
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11
Q

recognition and activation of innate immunity:
— pathogen associated molecular patterns
— pattern recognition receptors
— toll-line receptors
—– initiates inflammation
- antigen presentation occurs in —
—– instructive cytokines (secreted by apcs) that cause T cell differentiation —> — subset

A

PAMP
PRR
TLR
IL-1/TNF/IL8
IL-23
TH17

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12
Q

T17 are imprortat against extracellular bacterial infections and their function is:

A

*Recruits neutrophils
*Release of antimicrobial peptides
*Increased barrier integrity
( check slide 19 plsss)

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13
Q
  • Streptococcus pyogenes
  • Streptococcus pneumoniae
  • Staphylococcus aureus
  • Candida
    are all examples of —
  • IL-23 ( ustekinumab ) — > — which gives —
A
  • Th17 good and bad
  • TH17 –> IL-17 IL22 aka secrukinumb
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14
Q

b cell response to streptococci :
1-protein antigen as –>
- isotope switching leads to the production of — and — which is important for mucosal protection
- generation of —- cells which reside in the — and —
- production of — which resides in —- of —-
2- non protein antigens as—>
1- minimal isotope switching leading to — production for the complement activation
2- generation of — affinity and — lived plasma cells ( IgM isotope ) which reside in the – and — which is important for hyposplenism
3- no —

A
  • toxin
  • IgG and IgA
  • long lived plasma cells
  • bone marrow and gut
  • memory b cells
  • marginal zones of 2ndary lymph organs
  • lipoteichoic acid
  • IgM
  • low affinity
  • short lived plasma cells
  • spleen and musocsa
  • no memory cells
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15
Q

— will neutralise , activate compliment , and promote opsonisation
the —- are directed towards the — to prevent entrance but also towards —
- —- tags the streptococcus for — and — by —
- compliment activation triggers more — and —

A
  • antibodies
  • neutralising antibodies
  • streptococcus
  • exotoxin ( as strepyolysin O & S)
  • opposition
  • recognition ad phagocytosis
  • by macrophages
  • opsonisation and inflammation
    ( check slide 22 23)
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16
Q

—- is know as the reduction of splenic function
- the clearing of extracellular infections requires — whcih produced by —
- spleen is crucial — lymphoid organ where it:
— finish their development
— and — await for antigens circulating in the blood
- the short lived plasma cells for IgM antibody prdocudtion is —
causes of hyposplensim :
- reduced splenetic function leads to —- and then —

A

hyposplenism
antibodies produced by b cells
2ndary
b cells
t and b cells
stored
causes:
* Congenital absence of spleen (asplenia)
* Surgical removal of the spleen (trauma, autoimmune cytopenia, Lymphoproliferative disorder)
* Functional hyposplenism (Coeliac disease, Sickle-cell anaemia)
-Reduced splenic function →no short lived plasma cells for IgM
production →recurrent bacterial infection

17
Q

management of hyposplenism:

A
  • Management is aimed at reducing infection
  • Prophylactic antibiotics starting at birth (in case of asplenia) or
    after surgical splenectomy (life long)
  • Immunisation with vaccines 2 weeks prior to surgery or as early as
    possible
    – Polyvalent pneumoccal
    – Haemophilius Influenzae b
    – Meningitis C
    – Annual influenza
  • Annual measurement of antibody titers is recommended
  • Patient education – i.e. make sure they know they are at risk! They
    should be advised about risk of travel and insect bites + carry a
    splenectomy card or wear a medic-Alert bracelet
18
Q

—- initiates inflammation
antigen presentation occurs in —
—- instructive cytokine
that cause T cell
differentiation → –
subse

A
  • IL-1/tnf/IL-8
  • lymph nodes
  • IL-4
  • TH2
19
Q

—- are important for helminths infection and their function include:

A
  • TH2
    ( the IL-4 —> TH2 which gives IL4 IL5 IL13)
    Key Functions:
    *Isotype switching towards IgE & IgG
    *Recruits mast cells and eosinophils
    *Mucus production and intestinal
    peristalsis to expel helminth
20
Q

mast cells granules contain —- and
other substances that directly kill the worm
they secrete – which increases the secretion of — in the gut and helps — ( since mast cells help getting rid of the killed worm )
estinophil granules contain – that are toxic for parasites
the presence of — antibody help in cause of — infection

A
  • protease
  • histamine
  • mucos
  • peristalsis
  • proteins
  • IgE
  • 2ndary
21
Q

TH2 associated diseases:

A

Increased susceptibility to
Asthma and allergy:
High levels IgE
High levels mast cell activity
( check slide 30 pls)