'Lyme borreliosis should be considered in symptomatic patients that have
had exposure to ticks and not just those with a definite tick bite.'
Distribution and presentation of Lyme borreliosis in Scotland - analysis of data from a national testing laboratory.
Mavin S, Watson EJ, Evans R.
Abstract
Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection
Abstract
Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with B. burgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B.burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain ofB. burgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of B. burgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.
Although this study is more concerned about long lived Immunity it also highlights other problems with B cell or antibody responses - '“This study also suggests a possible mechanism responsible for the disappearance of antibodies following infection and subsequent treatment with antibiotics,”
'For months after infection, those germinal centers fail to produce the specific cells—memory B cells and antibody-producing plasma cells—that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections with the pathogen'
There have been comments made that as patients become more ill their antibody response weakens and the Embers monkey study found that in monkeys infected but left untreated their antibody response weakened or leveled off. Link to the study - http://lookingatlyme.blogspot.co.uk/2012/01/proof-of-persistence-chronic-lyme.html
Over twenty years ago antibody response to Borrelia were already recognised as being problematic.
Second European Symposium on Lyme Borreliosis
A NATO advanced research workshop held on 19 and 20 May 1993 at St George's Hospital Medical School,
University of London, United Kingdom
(Organising committee John S Axford and David H E Rees (co-chairmen), Allen C Steere, Klaus Hansen, Susan Henderson (administrator))
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1005059/pdf/annrheumd00480-0077.pdf
page 398
Even though Lyme disease has been clearly
identified as an infectious disease, there are
still many riddles to be solved, especially with
regard to the immune response to this
organism. These include the question why
only a small proportion of subjects originally
exposed to B burgdorfenr progress to later
disease stages, the genetic background, and
the apparent dissociation between the
cellular and humoral immune reactivity and
a tremendous, but nevertheless restricted and
apparently non-protective, antibody
repertoire.
Thus patients with
Lyme borreliosis showed a significantly
raised T cell response to whole B burgdorferi
bacteria as compared with patients with other
inflammatorv joint diseases and with normal
controls.
This dissociation of the humoral and the
cellular immune response may be explained
by several mechanisms. Initial experiments
using T cell clones in patients with chronic
Lyme disease suggest a selective activation of
a certain T cell subset that produces a
restricted pattern of cytokines which are
unable to activate B cells.6 This selective
expansion of responding cells may depend on
the HLA profile as suggested by the high
association of chronic Lyme arthritis
refractory to antibiotic treatment with certain
HLA-DR2 and DR4 alleles.7 In addition to
an unusual T and B cell response, there is a
peculiar uptake mechanism of B burgdorferi
by phagocytes, which may explain some of
the subsequent specific immune reactions.
page 399
It is an interesting finding that in the late
stages of spirochaetal diseases, such as
syphilis and, notably, Lyme disease, few
infectious organisms are detectable in the
lesional sites. There is often a strong local
immune response, however, with a
sometimes vigorous synovial inflammatory
hypertrophy in Lyme arthritis which is
histologically indistinguishable from rheumatoid
synovitis.9 Apparently, just a few bacteria
are sufficient to attract vast numbers of cells
to the areas affected. It may be either a
general immunosuppressive state that does
not allow for a complete elimination of the
microbe-or, alternatively, the immune
system is directed into the wrong direction
and uses false or inadequate means for
elimination. Thus the study of Lyme disease,
especially its arthritic manifestations, has
provided important lessons about an
inadequacy of the immune response towards
elimination of microbial organisms in a
chronic infection. These observations may
provide important insights into other
arthritides which are triggered by contact
with infectious agents.
There were some very interesting presentations made at this Symposium held in London but very little has followed in respect of translating this into meaningful help to protect the British public from the devasation of this disease.
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