NAC consultant Eavan Muldoon introduces herself as our new medic and talks a little about her background, part of which was spent at Tufts Medical Centre, Boston, USA. Then Graham Atherton talks about IgG, what they are and how they work.
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Comparing parts of UK & US Healthcare systems, IgG explained
1. LED BY GRAHAM ATHERTON
SUPPORTED BY
NAC CENTRE MANAGER CHRIS HARRIS
EAVAN MULDOON
CONSULTANT
THE NATIONAL ASPERGILLOSIS CENTRE
NATIONAL ASPERGILLOSIS CENTRE
UHSM
MANCHESTER
Support Meeting for
Aspergillosis Patients & Carers
Fungal Research Trust
2. Aspergillus meeting – Friday 20th
September 2013
Eavan Muldoon
Consultant in Infectious Diseases
5. Differences between the USA and UK
• Differences in healthcare provision
– Funding
– Structure of medical teams
– Clinics
– Number of doctors
• Differences in Management of Aspergillus
disease
7. Programme
1.30 Eavan Muldoon– NAC Consultant
2.00 Graham Atherton – Your subject (IgG)
2.30 Patients Discussion (Break)
3.00 Group discussion/Requests for information
ICAAC : A ‘sniffer’ for Aspergillosis
Patients survey
3.20 Q & A from the floor or online
8. Suggest a subject
Can be on any relevant subject you would like to hear
our opinion or get our help with
Send suggestions to admin@aspergillus.org.uk
Pass notes to me at clinic or at the meeting
Phone them in (24 hrs) at 0161 291 5866
9. IgE
Immunoglobulin E (IgE) – an antibody
Also have IgA, IgG, IgM – each plays a different role
IgE main role – defence against parasites!
Normally very low levels
IgE is released as soon as an infection is detected –
the hypersensitivity response. Gets all immune cells
ready for action – allergy!
11. Role in disease
Secondary Immune response (IgE Is part of the
Primary Immune response)
All happens in our Lymph nodes
The most abundant Ig in our bodies – making up
75% of all Ig molecules circulating
Made by B cells
Controls infection – bacteria, virus, fungus
12. Highly specific
Ends are HIGHLY variable so can recognise millions
of different molecules on the surface of foreign
bodies entering our bodies
13. Recognition & replication
Once attached the other end of the antibody
becomes very attractive to B cells, which will stick to
it.
This stimulates the production of more B cells
producing that specific antibody and each B cell
produces lots more antibody. This quickly produces
vast numbers of specific antibodies
All this activity is one reason why your lymph nodes
swell up when you have an infection!
14. Recognition & replication
Interestingly, the better the ‘fit’ (recognition) of the
antibody to the foreign particle (virus, bacterium,
fungus) the more intense the production of that
antibody, so the best antibodies quickly dominate.
Clever!
15. Vaccines
Once B cells go through this process they can
become ‘memory’ B cells with a long life – this is why
vaccination works.
In vaccined individuals, IgG appears about 24–48
hours after infection.
16. How do antibodies work?
Multiple mechanisms
IgG-mediated binding of pathogens causes their
immobilization and binding together via
agglutination;
IgG coating of pathogen surfaces (known as
opsonization) allows their recognition and ingestion
by phagocytic immune cells;
IgG activates the classical pathway of the
complement system, a cascade of immune protein
production that results in pathogen elimination;
IgG also binds and neutralizes toxins
17. Protection of new born child
IgG is small in size allowing it to easily perfuse tissues.
It is the only isotype that can pass through the human
placenta, thereby providing protection to the fetus in utero.
Along with IgA secreted in the breast milk, residual IgG
absorbed through the placenta provides the neonate with
humoral immunity before its own immune system
develops.
Colostrum contains a high percentage of IgG, especially
bovine colostrum.
18. What do your tests mean?
If you have large amounts of IgG circulating in your
blood, you probably have an ongoing infection (not
allergy!)
If we can identify the specific type of antibody as
being one that attaches to a specific bacteria, virus or
fungus then it tells us which organism is causing the
infection.
Useful!
25. Any other Immunoglobulins?
IgM – very large, found in spleen. Good indicator of
very recent infection. Good at binding infecting
particles even if no prior immunity! Blood
agglutination is mainly caused by this Ig
IgA – Important in the mucosal lining of our organs,
the main immunoglobulin found in mucous
secretions, including tears, saliva, colostrum and
secretions from the genitourinary tract,
gastrointestinal tract, prostate and respiratory
epithelium. Highly resistant to breakdown in gut.
IgD – found in small amounts in blood.
26. ICAAC 2013: Aspergillosis ‘sniffer’
An Aspergillus fumigatus (AF)-Specific Breath Volatile
Organic Compound (VOC) Profile is Diagnostic of Invasive
Aspergillosis (IA)
Sophia Koo, MD; Brigham & Women’s Hosp., Boston, MA
Poster Session 023, Presentation M-219
The suggestion is that this research will enable us to
diagnose invasive aspergillosis by testing the breath of the
patient. This would be a useful tool (if reliable and
accurate) as diagnosis of IA is currently slow and difficult,
and even more importantly all delay in the diagnosis of
invasive aspergillosis has the effect of increasing mortality
rates. The sooner we are able to start treatment the better!
34. Has the move to Friday Meetings worked?
8 months prior to move - 32 patients/carers
attended
8 months after move - 42 patients/carers attended
(32% increase)
Total numbers of visits have also risen 15 - 20%
=Success! Any other ideas?
Over the whole history of the meetings (3 years),
over 150 patients/carers have attended.