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| | | From: Rene (Original Message) | Sent: 2/8/2006 4:55 PM |
Mysterious Lyme M. Linton, Sun Media, July 4, 2005 The story of Keith Poullos sounds like one of those medical mystery scripts you'd see on something like TV's House, where Dr. House works through a series of theoretical medical mazes in an attempt to track down whatever it is that, within 10 minutes of t TICK-TOCK ... Lyme disease is transferred after a tick has attached itself for 36 to 48 hours.
In Poullos' case, the cause of his symptoms (which included fatigue, brain fog, body pain, numbness and stuttering, to name a few) was so elusive it looked as if he might have anything from MS to Alzheimer's, from fibromyalgia to depression. Instead, the cause was a tiny critter called the deer tick and the final diagnosis was Lyme disease. Poullos, who lives just northwest of Toronto and works as a small engines mechanic, feels the disease has been overshadowed by the awareness of West Nile Virus and that doctors just don't get it. "My doctor knew nothing about it and didn't think it was a problem here," he said. "They all think it's an American problem. The doctors are just not educated on this, in this country." After no help at all from the medical community, Poullos was advised by a veterinarian to pressure his doctors to consider Lyme disease. He's now on antibiotics and feels greatly improved over a few months back. Lyme disease is actually the most commonly reported tick-borne illness in the U.S., having been identified in 1975 after a clustering of cases around Lyme, Conn. The ugly miniscule creatures, about the size of a sesame seed, attach to the skin and, if they themselves are infected by a bacteria called Borrelia burgdorferi and remain on the skin feeding on your blood for between 36 and 48 hours, you will also become infected. The classic tick bite sign is a bulls-eye type rash that develops around the initial bite site between three and 32 days. Flu-like symptoms, fatigue, chills, fever, headache, a stiff neck and a general malaise, accompany the illness. And although a course of antibiotics can cure it, patients who've struggled with the illness say too few doctors diagnose it in the first place. That may be because the test available to confirm the diagnosis (called an ELISA test) is unreliable, and a second more reliable test (called the Western blot) is used only if you test positive with the ELISA, says B.C.'s Jim Wilson, president of the Canadian Lyme Disease Foundation (www.canlyme.com), and a Lyme disease patient. He believes the more sensitive Western blot should be used more often: "A survey of 516 labs showed that they all failed to detect Lyme disease using the ELISA method," he said. Wilson also criticizes Canada for doing a dismal job of tracking the disease: "The confirmed cases in Ontario are 23 a year. Across the border, however, they have 5,000 cases a year. Yet we share the same fauna and flora as our neighbours to the south. The migratory birds transplant these ticks everywhere, they are like airplanes for the ticks. "In the U.S., they have a surveillance system and wherever they look they find it. The doctors also look for it. Here, doctors say: 'Don't be silly. Your symptoms aren't Lyme disease �?it's too rare.' That same patient goes across the border to a doctor and the doctor will diagnose Lyme. Here it's not even on the radar." Wilson further charges while Canada's "medical machine continues to deny the true prevalence of this disease, more and more evidence is mounting that it may be a pandemic." He says there were over 23,000 cases confirmed in 2003 in the U.S. and Lyme is underestimated "six to 12 fold." However, others argue fewer than 15,000 North Americans annually are affected. If indeed it is an enormous public health issue, we're sure to hear about it soon. But even if it isn't, more of us need to be aware of the long-term danger of the disease. Recent Finnish research indicates nearly one-third of people with Lyme disease do not show immediate symptoms. Instead, the bacteria multiplies within the body �?hiding sneakily from the immune system, and eventually wreaking havoc on the body's defences. Wilson says it was months after he was bitten in 1991 that he experienced drooling, numbness in his legs, and foggy thinking. Part of the frustration felt by Keith Poullos is he could have been bitten decades ago. Later stages of Lyme disease can include nervous system disorders, abnormal pulse, enlarged lymph glands, facial palsy and arthritis. Prevention is key. Use insect repellents containing DEET and cover up with long pants and long-sleeved shirts. If you do see a tick, don't panic; infection is unlikely to occur before 36 hours of tick attachment. It's important to check daily for ticks. If you find a tick the Canadian Lyme Disease Foundation says to promptly remove it with fine-tipped tweezers, getting as close to the skin as possible, then cleanse the area with an antiseptic. Ticks prefer moist, shady places with low-lying vegetation, overgrown grass or leaf litter: Think woods and the edges of rural golf courses. But these creatures cannot jump or fly, so you'll only get one on you if you happen to brush against it. So don't get ticked: Skin cancer isn't the only reason to cover up this summer. http://www.calgarysun.com/perl-bin/niveau2.cgi?s=Lifestyles&p=96859.html&a=1
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| | | From: Rene | Sent: 3/19/2006 2:18 AM |
5 February 2006
ONE CLICK ANNOUNCEMENT - BORRELIOSIS The One Click international pressure group founded in 2003 by Jane Bryant and Angela Kennedy was originally set up to assist sufferers of the neurological disease ME/CFS, classified as such by the World Health Organisation under ICD-10 G93.3, because our children had been diagnosed with this illness. It has now been found that our children have borrelia spirochaetes - chronic Borreliosis. For information on the chronic Borreliosis issue, see here: Lyme disease - ancient engine of an unrecognised borreliosis pandemic
http://www.theoneclickgroup.co.uk/documents/Borreliosis/Lyme%20disease,%20borreliosis%20pandemic.pdf NHS National Library for Health - Diagnosing Lyme disease
http://www.clinicalanswers.nhs.uk/index.cfm?question=1076 Our children were originally misdiagnosed and have suffered greatly and needlessly for years. If our children had been properly diagnosed and treated appropriately at the beginning of their illness, things would have been very different for them and for us. Borreliosis is treatable. However, if the infection is allowed to proliferate unchecked and untreated for many years as is the case with our children, the treatment road is hard. The symptoms of chronic Borreliosis and ME/CFS are to all intents and purposes, the same. The fact that our children have chronic Borreliosis means that they are excluded from being labelled and diagnosed as ME/CFS sufferers by the exclusion clauses of all the ME/CFS criteria currently in use, including the Oxford, Fukuda/CDC and Canadian criteria that prevent an ME/CFS diagnosis if a chronic infection is present. Any sensible reader will know that the situation is far more complex than this and we will therefore continue, where appropriate, to advocate for all groups of people with organic disease adversely affected by the psychiatric paradigm conducted by psychiatrist Simon Wessely et al. We would recommend that anybody interested in the issue of Borreliosis should visit the EuroLyme group at: http://health.groups.yahoo.com/group/EuroLyme In light of this new chronic Borreliosis diagnosis in relation to our children, the One Click international pressure group will now widen its remit and will provide opposition to the psychiatric paradigm for patients suffering from diseases such as Gulf War Syndrome, Lyme disease/Borreliosis and ME/CFS. We will continue to carry breaking news, information and archive resources on these issues. Jane Bryant & Angela Kennedy
The One Click Group http://www.theoneclickgroup.co.uk/
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Reply
| | | From: Rene | Sent: 7/2/2006 1:57 AM |
Sleuthing Lyme. More than 25,000 people in the United States contracted Lyme disease in 2005,
but the actual number of cases, the Centers for Disease Control and Prevention concedes, may be
10 times higher than that. The numbers for Lyme disease in California are three times higher for
2005 than for the previous year. Despite that fact, the CDC recently warned the public that some
private medical laboratories may be overdiagnosing positive results of Lyme disease to better
their business.
Long-term Lyme disease can be debilitating, including body aches, neurological damage and even
loss of sight. Its symptoms are often misdiagnosed or confused with those of other diseases such
as fibromyalgia, Parkinson's disease, Lou Gehrig's disease or multiple sclerosis, the medical
literature refers to it as "the great imitator."
FULL STORY: |
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Reply
| | | From: Rene | Sent: 1/16/2008 10:59 PM |
The Pathogenesis of Lyme Neuroborreliosis - from Infection to Inflammation -
Source: Molecular Medicine, Dec 19, 2007
by Hans-Walter Pfister, MD, et al.
ProHealthNetwork.com 01-15-2008 [Note: The full text of this article may be accessed free at PubMed Central [http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18097481]. It includes illustrative figures and links to more than 100 footnoted references. This review describes the current knowledge of the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central nervous system.
Borrelia burgdorferi (B.b.) enters the host through a tick bite on the skin and may disseminate from there to secondary organs, including the central nervous system.
To achieve this, B. b. first has to evade the hostile immune system.
In a second step, the borrelia have to reach the central nervous system and cross the blood-brain barrier.
Once in the cerebrospinal fluid (CSF), the spirochetes elicit an inflammatory response.
We describe current knowledge about the infiltration of leukocytes into the CSF in LNB.
In the final section, the mechanisms by which the spirochetal infection leads to the observed neural dysfunction will be discussed. In conclusion, this review will construct a stringent concept of the pathogenesis of LNB. Source: Molecular Medicine. 2007 Dec 19. PMID: 18097481, by Rupprecht TA, Koedel U, Fingerle V, Pfister HW. Departments of Neurology and Microbiology, Ludwig-Maximilians University, Munich, Germany prohealth.com Treatment & Research Information
Excerpts: Introduction Lyme borreliosis is the most common human tick-borne disease in the Northern hemisphere. Its prevalence is estimated to range between 20 and 100 cases per 100,000 people in the US and about 100 to 130 cases per 100,000 in Europe (1;2). It is caused by the spirochete Borrelia burgdorferi (B.b.) sensu lato. B.b. can be divided into four human pathogenic species: B.b. sensu stricto (the only human pathogenic species present in the US), B. afzelii, B. garinii and B. spielmanii (3). The infection by B.b. is a complex process beginning with the translation from the gut to the salivary glands of the tick during the feeding process on the host. After invasion into the skin, B.b. can cause a local infection called erythema migrans (EM). During the second stage of Lyme disease, B.b. can spread from the tick bite on the skin to various secondary organs throughout the body, including the heart, joints, and the peripheral and central nervous system (CNS) (4). Major clinical findings of the neurological manifestation of acute Lyme neuroborreliosis (LNB) include painful meningoradiculitis with inflammation of the nerve roots and lancinating, radicular pain (Bannwarth’s syndrome), lymphocytic meningitis, and various forms of cranial or peripheral neuritis (5).
While the clinical picture of painful meningoradiculitis was first described in 1922 (6), the etiology was unknown till the description of the causative spirochetes by Willy Burgdorfer et al. in 1982 (7), and the isolation of spirochetes from the CSF of a patient with Bannwarth’s syndrome in 1984 (8). During the last 25 years we have gained some insight into the pathogenesis of LNB, but there are still many aspects that have not yet been clarified. One reason for our incomplete understanding of the mechanisms that lead to LNB is the limited availability of an adequate animal model. The induction of a reliable, clinically manifest LNB in an animal model so far was only successful in a nun-human primate model involving the rhesus macaque, where for example, spirochetes could be demonstrated at the nerve roots (9). Further insight has been gained either from human material or cell culture experiments: while for example the inflammatory response of the human host to B.b. has been measured in CSF samples (10�?2), the mechanisms of adherence of B.b. to endothelial cells, cytotoxicity on neural cells, or the induction of cytokines was analysed using primary cells or cell lines in vitro (13�?7). Though our knowledge of the pathogenesis is still incomplete, this review attempts to construct a stringent concept of the pathogenesis of LNB, from the first encounter of the spirochetes with the hostile immune system inside the tick up to the neuronal dysfunction evoked by B.b. as seen in patients with LNB.
Hiding from the immune system
Even before entering the host, the spirochete has to evade the hostile immune system. During the first 24�?8 hours of tick feeding, the borrelia are attached to the tick gut, mediated by the interaction of the borrelial outer surface protein A (OspA) with the tick receptor for OspA (TROSPA) (18). While the hostile blood flows into the tick gut, the spirochetes multiply and prepare for dissemination to the salivary glands (19). At that time, the borrelia are already faced with the different components of the mammalian immune system. An impressive example of this is the mechanism of action of OspA vaccination: anti OspA antibodies from the host are able to kill the borreliae already in the tick gut, thereby preventing infection of the host (20). In parallel, the borrelia are confronted with the hostile complement system. The complement system is a biochemical cascade which is not only potentially cytotoxic, but also opsonises the pathogen and attracts leukocytes (21). The leukocytes constitute another threat for B.b.: different borrelial surface lipoproteins are recognized by leukocytes, mainly by CD14 and the toll-like receptor 2 (TLR2) of the innate immune system (17;22�?4), and it has been shown in vitro that the spirochetes are rapidly taken up by polymorphonuclear cells, monocytes, and macrophages (25�?7). Once having entered the host, there are further hazards for B.b., especially when seroconversion has taken place, as mouse and human antibodies against different outer surface proteins (for example OspA or OspC) are borreliacidal in vitro (28;29). However, though the mammalian immune system possesses several means to defend itself against the borrelial invasion, the elimination might be incomplete. Without the application of antibiotics, B.b. might persist in the mammalian host, chronic infections have been reported in the literature (5;30) . But why is it so hard for the immune system to attack the borrelia? To achieve this, the borrelia possess several mechanisms which enable them to escape (Figure 1) by: (I) downregulation of immunogenic surface proteins, (II) inactivation of its effector mechanisms, or (III) hiding in less accessible compartments like the extracellular matrix. This will be depicted in detail below. Downregulation of immunogenic surface proteins. To escape from the immune reaction of the host, the borrelia hide highly immunogenic surface proteins using the mechanism of antigenic variation (31). OspA, for example, is a potent stimulator of neutrophils (32) and induces the release of proinflammatory cytokines like Il-1β, TNF-α or IL-6 in vitro (33). To avoid such an inflammatory response, OspA, while abundantly expressed in the tick gut as an important adhesion protein (34), is rapidly downregulated during the feeding process on the host (35;36). Though OspA positive Borrelia are able to enter the host, they are unable to establish an infection (37) and B.b. isolated from mice four days after infection are all OspA negative (38). It can be concluded from these results that only OspA negative Borrelia are able to survive in the host and therefore, this surface protein does not appear to be expressed during the early phase of the infection. OspC, in contrast, is rapidly upregulated before dissemination to the salivary glands during the blood meal of the tick, most probably mediated by the increasing temperature and the pH shift as the blood of the host enters the tick gut (39�?1). The expression of OspC constitutes an important initial survival factor during transmission from the tick to the host: In a recent study, it has been shown that B.b. can bind the complement inhibiting protein Salp15 of the tick saliva via OspC, which protects the spirochete against the hostile complement system (42). Therefore, the expression of OspC appears essential for the first 48 hours of infection to escape the innate immunity (43) and OspC negative Borrelia are unable to disseminate and invade the host. However, a persistent infection of the host is only possible by downregulating OspC again 8�?1 days after infection (44). A constitutive expression of OspC, as for example, by a mutation of the respective regulatory element, leads to an efficient clearance of the borrelia once the humoral immune response is set (44;45). Therefore, the borrelia also hide this surface protein later during the course of infection to remain unrecognized from the immune system of the host. This is supported by the finding that Anti-OspC antibodies are found in the rhesus monkey up to 20�?0 days after infection, while they disappear in later stages (46). In parallel, neither OspA, nor OspC expression can be found in persistent borrelial infection in the rhesus monkey, and the rate of systemic inflammation in these animals is low (47). All in all, it appears that the borrelia suppress or hide several surface markers in order to minimize their immunogenic characteristics, but a transient expression can be used to utilize protective mechanisms. ............ Furthermore, Borrelia lead to a local upregulation of the matrix metalloproteinase-9, that digests the surrounding extracellular matrix (65). In addition, the borrelia can attach to several proteins of the extracellular matrix, such as, for example, fibronectin (66), several integrins (67), or proteoglycans like decorin (68). Decorin is a collagen-binding proteoglycan that is produced as a component of the connective tissue. It facilitates both the dissemination and the survival of Lyme disease-spirochetes in decorin-rich tissues (69). As a consequence, the borrelia can hide in these extracellular structures, rendering them less subject to the circulating leukocytes.
All these well orchestrated mechanisms may help the borrelia not only to survive, but also, for example by degrading the extracellular matrix, to disseminate in the host (69). There are two alternative ways for the spirochetes to reach the central nervous system from their original point of entry, the skin: either through the bloodstream, or along other structures like the peripheral nerves. There are several arguments that favour a dissemination of the spriochetes predominantly by the blood vessel route. First of all, the bloodstream is a well-known route of dissemination for many bacteria in the host and it is therefore likely that B.b. might also use this path. In accordance with this, borrelia can be cultivated in up to 35�?5% of plasma samples from patients with early Lyme disease in the US (70;71). It has to be kept in mind that the effective prevalence of borrelia in the blood of patients will be even higher, as the sensitivity of culture methods can never achieve 100%. Therefore, hematogenous dissemination of the spirochetes can be considered frequent in patients with Lyme disease in the US (71). The exact mechanisms by which the spirochetes travel through and along with the blood and escape the circulating immune cells are not known. Though it would be tempting to speculate that they bind to the integrins on the surface of circulating platelets, it is rather unlikely that spirochetes can use them as a sort of protected transport vehicle, as activated platelets are not abundant in the circulation (72). After they have arrived at the cerebral or spinal vessels, the borrelia might attach to the endothelial cells by inducing adhesive proteins like E-selectin, ICAM-1 or VCAM-1 (73), or they can bind via integrins (67) to a localized aggregation of activated platelets (72). One of the borrelial proteins that could be involved in this adhesion process is, as in the tick gut, OspA: antibodies against this surface protein could significantly reduce the adherence to endothelial cells in vitro (13).
However, it has to be kept in mind that OspA was found to be downregulated during dissemination in the host (37;38), and therefore, the relevance of this in vitro finding for the in vivo situation would have to be clarified in further studies.
It is still a matter of debate how the borrelia passes the blood-brain barrier. While some authors argue for a penetration of the spirochetes between the endothelial cells (74;75), others favour a transcellular passage (76). Even though the exact mechanism is not yet clarified in detail, the definite entry of borrelia into the cerebrospinal fluid was documented by both culture methods and PCR (3;8).
......
Conclusion
The pathogenesis of LNB is a complex process with several fascinating aspects, such as, for example, how the borrelia manage to escape the immune system and the ability of the spirochetes to invade the carefully protected CNS. Insights into the pathophysiology of this disease help us to understand the principal microbiological mechanisms involved and these insights might even be transferable to infections with other spirochetes like Treponema or Leptospira. Therefore, further research on the pathophysiology of infection with B. b. would increase not only the knowledge of Lyme borreliosis but also of other spirochetal diseases, with an increasing incidence and higher morbidity and mortality, like syphilis or Weil’s syndrome.
[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18097481]
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