ref confused - its absolutely understandable - lyme testing via serology is a complex and problematic subject.
ref thinking IgG is from long standing exposure / past infection and IgM from recent / current
here is some info i posted a while back
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On serological testing for Lyme and IgG / IgM
one of the main problems with serology based tests for lyme - is that you are measuring a secondary effect - ie "how is the patient’s immune system behaving?"
not a direct test "can we detect the bacteria?"
in Lyme - there are countless studies showing that the very thing you are measuring with serology (how the patients immune system is responding) is itself disrupted by the Lyme infection - and as a result it no longer functions the way its expected to - and does not produce the pattern of IgG or IgM antibodies that are expected in most* other infections.
in all other disciplines this flawed approach would be classed as crazy logic and thrown out the window
in Lyme testing there are few alternatives - and so we are kinda stuck with it - even though it is flawed.
for example - there are papers finding that around 20% of patients with confirmed lyme infection by culture ( gold standard test method but rarely used) NEVER produce ANY detectable anti-lyme antibodies at all. So this makes it clear that lyme interferes with normal expected antibody production.
more often with lyme disease - and what you will often see if you read other people’s accounts here on the forum is:
- there is general poor sensitivity of basic C6 ELISA tests ( this is the general first line test used in many countries - and looks for only one antibody) – as a result often just a negative result is reported and no further tests done.
- and on western blots / immunoblots - some kind of random selection of a few IgG and IgM antibodies or a few indeterminate - rarely the full suite of antibodies that many conventional doctors insist on for a positive diagnosis.
the main reason for this is the immune disruption mentioned above
however, borrelia also have a key feature v few other microbes have - in that they change the proteins expressed on their outer surface regularly - it is these outer surface proteins that the immune system reacts to and makes antibodies to - so this means the immune system has to keep relearning how to recognise them and then make new antibodies to the latest outer surface protein - this is the explanation for reoccurring IgM antibodies in chronic lyme infection.
there is ongoing confusion where people, including doctors, apply general rules of thumb learned from testing other simpler organisms - which have altogether different biology (it is in fact the most complex bacteria with the largest genome of any bacteria so far discovered by quite some margin) and so those simplistic explanations used as rules of thumb for much simpler organisms do not fit borrelial infections well at all.
*I say most as, in many chronic bacterial infections (especially those in the co-infection group) expected antibodies are often not present after 6 months - the mechanisms for this are also not clear in all cases, but likely due to some immune evasion or immune suppressive effects the organisms have developed over the millennia to aid their chronic infection survival strategy – after all killing the host is no good for survival - and getting mopped up by the host immune system is no good either - so they have to find something in between. That in between way involves some form of manipulation of the host immune system by the microbe in all chronic infections.
More detail on IgM vs IgG in lyme
the lyme disease organism has the one of the largest genomes ( amount of genetic code) of any bacteria so far discovered.
the large majority of this extra genetic material, compared to more regular bacteria, is dedicated to making different outer surface proteins
this enables it to change the proteins it has on its outer membrane - this is important as these are the ones the immune system is in contact with and trying to make antibodies to, which takes time - maybe 1 month and are initially IgM antibodies ( it later learns from these IgM antibodies what to make IgG antibodies to )
by the time the body has figured out what proteins to make antibodies to the organism has changed the proteins in the outer membrane and now looks like a new infection to the immune system - and so off the immune system goes again, trying to make new (IgM) antibodies to that - and so the cycle continues.....
you can see what an effective an immune avoidance mechanism this is - as the body never quite catches up to the microbe with its learned immunity.
you can also see how this would result in IgM antibodies being present on an ongoing basis in chronic infection
it is not always this way however - as the organism also has other immune disrupting strategies and one of these is it interferes with the body’s ability to make antibodies at all - and so we instead tend to see a somewhat randomised picture of: no antibodies, only IgM antibodies or a random mix of IgG and IgM antibodies on western blots in people with Chronic Lyme disease.
Post Edited (Garzie) : 1/31/2023 3:39:11 AM (GMT-8)