Saturday, 7 November 2015


'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.


This study examines the distribution of laboratory-confirmed cases of Lyme borreliosis in Scotland and the clinical spectrum of presentations within NHS Highland. Methods General demographic data (age/sex/referring Health Board) from all cases of Lyme borreliosis serologically confirmed by the National Lyme Borreliosis Testing Laboratory from 1 January 2008 to 31 December 2013 were analysed. Clinical features of confirmed cases were ascertained from questionnaires sent to referring clinicians within NHS Highland during the study period. Results The number of laboratory-confirmed cases of Lyme borreliosis in Scotland peaked at 440 in 2010. From 2008 to 2013 the estimated average annual incidence was 6.8 per 100,000 (44.1 per 100,000 in NHS Highland). Of 594 questionnaires from NHS Highland patients: 76% had clinically confirmed Lyme borreliosis; 48% erythema migrans; 17% rash, 25% joint, 15% neurological and 1% cardiac symptoms. Only 61% could recall a tick bite. Conclusion The incidence of Lyme borreliosis may be stabilising in Scotland but NHS Highland remains an area of high incidence. Lyme borreliosis should be considered in symptomatic patients that have had exposure to ticks and not just those with a definite tick bite.

Thank you Scotland another insightful piece of research in this very important field.

Not everyone recalls a tick bite and not everyone gets an Erythema Migrans rash.

Currently there is much debate over the inadequacy of the current testing,  a two tired system of testing antibodies called the ELISA and the Western Blot.

This is an interesting paper 

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection


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 Bburgdorferi 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 Bburgdorferi 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 ofBburgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of Bburgdorferi, 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 Bburgdorferi-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 -

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))
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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