This report is a whopping 485 pages.
I don't have the focus required to get through the entire thing in one sitting, and it would take me a long time to write up a comprehensive summary that hit on what others may want to hear.
Besides, from the patient perspective, the big bullet points about how well the workshop went in terms of advocacy and awareness and the follow-up summary report have already been covered by Lyme Policy Wonk, NatCapLyme, and others.
So I'm going to take another approach here, and write about specific topics I pick out of the report and cite them.
The focus of this post will be Neuroborreliosis, which means when Lyme disease infects the CNS and brain.
I find it interesting to juxtapose the comments I see made by someone in discussion in one part of the report and then in the research portion of their report, information which at least partially contradicts what was stated.
Let me show you what I'm talking about here...
For example, page 9-12 has as part of the end of workshop discussion stating the following:
"A question was raised about who should comprise a clinical management team to treat patients with long-term symptoms. O’Connell noted that Lyme disease affects a number of different systems, depending to some degree on the borrelial genospecies causing the infection.Borrelia burgdorferi, which is the most common strain in the United States and also occurs in Europe, tends to cause Lyme disease arthritis. Borrelia garinii, which is strongly associated with neuroborreliosis, and Borrelia afzelii, mainly causing skin manifestations, are more common causes of Lyme borreliosis in Europe."
And when you read page A-180, Susan O'Connell has this to say:
"Although the differences between presentations of European and American Lyme neuroborreliosis have been stressed over the years, they may have been overemphasised in the case of early neuroborreliosis (Halperin, 2008). This is also supported by clinical experience in the UK, where between 10 and 20% of patients with serologically confirmed Lyme borreliosis acquired infections abroad, in mainland Europe or USA (HPA, 2011). Clinicians in the UK have noted marked similarities in acute neurological presentations of patients with USA-acquired infection and those acquired in the UK and other parts of Europe (Dillon, O'Connell and Wright (2010)."
In reading this, what is the reader to assume? Based on this information, it would appear that American patients suffering from a Borrelia burgdorferi infection could also be more likely to have acute neurological presentations - because if traveling Europeans are coming back from the US having received a tick bite in an endemic area, what are the odds they are showing an acute neurological presentation from an imported strain of B. garinii or B. afzelii? According to information presented elsewhere in this report, evidence of those strains in the US has been very isolated and found only in ticks in the southeastern portion of the US.
I also found this to be interesting information on patients in Europe, on page A-178:
"Neuroborreliosis has been notifiable in Denmark since 1994; with an annual average of 83 cases (1.5/100,000), ranging from 41 in 2002 to 104 in 2006 (Christiansen and Mølbak, 2005) and 61 cases (1.1/100,000) in 2009 (EpiNorthData, 2011). Cases of disseminated and late borreliosis have been notifiable in Norway since 1995. Annual incidence of neuroborreliosis varied from 75 to 200 cases in the ten years 1995-2004 (average 3/100,000), with a marked increase of nearly 100 cases between 2003 and 2004 (Nygard et al., 2005). There were 273 notifications in 2009, a rate of 5.6 /100,000 (EpiNorthData, 2011). As neurological complications are the most significant manifestations of disseminated and late Lyme borreliosis in Europe data on neuroborreliosis obtained from the Slovenian, Danish and Norwegian notification schemes can give useful information on epidemiological trends in widely geographically separated areas of Europe."
So, in Denmark, Neuroborreliosis is actually treated as a diagnosis which is medically notifiable separate from non-Neuroborreliosis Lyme disease - and in Norway, disseminated and late borreliosis are also notifiable there.
If there is evidence patients are returning to Europe having been infected with Borrelia burgdorferi in US, and they develop neuroborreliosis and it's reportable in these countries, one would think they have a better epidemiological picture than the US does about neuroborreliosis as well as greater awareness.
I don't know, though - I'm not living in Denmark, Norway, or Slovenia. So perhaps someone who is and reading this could leave me a comment on this issue.
At any rate, at least by characterizing diagnosis in this way and tracking this data, one would think that those patients who are not found to be positive by serological testing early in their infection or when early diagnosis of infection is missed that these cases of Lyme disease will be counted later on for a bigger epidemiological picture.
If there is great concern about the significance of neuroborreliosis in Europe, why aren't all countries adopting the reporting schemes these countries are using?
So here's an interesting counterpoint...on page A-180, the following is stated:
"Less than 5% of European neuroborreliosis patients present with late neuroborreliosis with duration of symptoms from six months to several years (Mygland et al., 2010). This condition is likely to have a chronic course if left untreated and can affect the central and peripheral nervous system."
And prior to this, on page A-179, the following is stated:
"Neuroborreliosis accounts for between 10% and 20% of laboratory-confirmed cases each year and appears to be a useful sentinel for year-on year comparison. It has been estimated that there may be 2,000-3,000 cases of Lyme borreliosis annually in the UK (Health Protection Agency, 2011)."
So, to make a distinction here - if I'm reading this correctly - O'Connell is saying that 5% of all European neuroborreliosis patients present with late neuroborreliosis, but the overall percentage of cases of neuroborreliosis reported is 10-20% of all reported Lyme disease cases.
Also on that same page, it is stated:
"The EUCALB case definitions acknowledge similarities between the major manifestations of Lyme borreliosis and North America, including erythema migrans, early neuroborreliosis and Lyme arthritis."
This is the piece that, between what I cited earlier and now concerns me: When Lyme disease is discussed in the US, many medical advice sites and articles written about Lyme disease seem to focus on it being a mild, flu-like illness where Lyme arthritis can develop if it's not treated early on.
And I think that may be how it is for a segment of the patient population who has an uncomplicated case, one involving a clear EM rash, and no coinfections, where one receives antibiotics soon after infection.
My concern is that the frequency of neuroborreliosis isn't something we're tracking that well in the US - and maybe it is being undiagnosed or misdiagnosed with other conditions.
Does anyone know how we track and record neuroborreliosis cases in the US? Or follow up on patients with tick bites who may not have shown symptoms immediately after the bite and only got a prophylactic dose of Doxycycline?
Regardless of anyone's thoughts and feelings about long-term antibiotic treatment, by missing a neuroborreliosis diagnosis early on, everyone is harmed by it - the patient, the patient's family and caregivers, the patient's workplace, and society in general. Without greater awareness, there is a risk of the diagnosis turning into something far more devastating, and the Lyme disease going untreated.
If anything the push to diagnose Lyme disease early on is just one piece of the prevention of long-term chronic symptoms related to Lyme disease - the push is to really be sure one catches neuroborreliosis early because that is often where the worst problems start.
On page A-180, it is stated:
"Central nervous system manifestations of late neuroborreliosis include encephalitis or encephalomyelitis with tetraspastic syndrome, spastic-ataxic gait disorder and disturbed micturition, which may lead to misdiagnosis with other conditions such as multiple sclerosis if the possibility of neuroborreliosis is overlooked.Clinical awareness of this possibility is crucial, as antibiotic treatment will arrest progression. The degree of clinical recovery following microbiological cure depends on the severity of tissue damage. Recovery may be slow, especially in older patients, and can be incomplete, particularly in those who had been severely affected prior to treatment."
And on page A-182...
"In neuroborreliosis only about 10-30% of DNA detection tests on CSF are positive, and highest rates are obtained on samples taken within the first two weeks of a clinical presentation. It is considerably more sensitive than culture for synovial tissue and fluid, for which culture has rarely been successful (Wilske et al., 2007)."
So just to lay this all out there for the reader, here you have a disease that can infect the brain early in infection and the infection cannot be detected in the CSF by using a DNA detection test anywhere from 70-90% of the time.
If you get bitten by a tick, and show symptoms of neuroborreliosis and get a lumbar puncture test to look for Borrelia DNA within the first two weeks of symptoms, then you have a better chance of getting a solid diagnosis. But once that window closes, then it will be harder to get a positive CSF reading.
This tip on page A-183 may help in diagnosing patients with neuroborreliosis after that two week window:
"Lymphocytic pleiocytosis is almost always present in both early and late neuroborreliosis and many patients have raised protein and oligoclonal IgG bands."But in using this diagnostic measurement, one has to make sure that the medical professional is willing to consider neuroborreliosis as a differential diagnosis and run an IgG test and not just a general test to determine if a patient has bacterial or viral meningitis when they actually have neuroborreliosis.A negative test for bacterial meningitis will be labeled as viral when it might have been neuroborreliosis all along.
You'd better have a good diagnostician in your corner who knows what you have and will treat it, because neither a CSF test nor a blood test has a good chance of returning a positive result for neuroborreliosis in early and early disseminated Lyme disease infection.
Continued at: Part 2: IOM Summary Report: Neuroborreliosis Notes
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