joe the tick

November 18, 2009

Imaging Technique Leads to Better Understanding On How Ticks Transmit Lyme Disease

Filed under: Lyme Disease, Lyme Disease Research — Tags: , , — joethetick @ 10:21 am

ScienceDaily (Nov. 17, 2009) — Using a powerful microscopic live imaging technique, a research team led by Dr. Justin Radolf, professor in the Departments of Medicine and Genetics and Developmental Biology at the University of Connecticut Health Center, has discovered the way ticks transmit Lyme disease to humans is different than previously thought. The research is published online in the Journal of Clinical Investigation.

Lyme disease is caused by transmission of the spirochete bacterium Borrelia burgdorferi from ticks to humans but for a number of technical reasons, the transmission process has been difficult to study.

Radolf and researchers Star Dunham-Ems and Melissa Caimano tried a novel approach. They genetically modified a virulent strain of B. burgdorferi to express green fluorescent protein (GFP). “This bacterium glows and can be followed in the living state as it migrates through the tick to the mouse during feeding,” explains Radolf. “Then using a powerful microscopic technique called confocal microscopy, we discovered that the transmission process unfolds quite differently than previously believed.”

Spirochetes in culture are highly motile, and it is widely believed that during feeding, the spirochetes in the midgut rapidly move through the wall of the midgut. But Radolf and his team found that during much of the feeding period, the spirochetes do not move. They actually divide and surround the cells of the midgut lining or epithelium, forming tight networks. “We also found that the reason they don’t move is that the tick midgut secretes molecules that actually inhibit the motility of the spirochetes,” explains Radolf.

Eventually, spirochetes in the networks reach the base of the epithelium by completely surrounding the epithelial cells. At this point, they become motile, detach, and completely penetrate the midgut, although in very small numbers. These few bacteria then swim to the salivary glands, which they penetrate en route to the mouse. “So rather than being entirely motility-driven, dissemination of spirochetes within ticks actually happens in two phases,” says Radolf, “which is something we didn’t know before.”

Lyme disease is the most prevalent vector-borne infection in the United States with more than 25,000 new cases reported annually. A substantial percentage of these cases occur in Connecticut. “The improved understanding of the transmission process revealed by our study could lead to novel strategies for controlling the spread of Lyme disease,” says Radolf.

November 11, 2009

LIVING WITH LYME: A phenomenally complex disease

Filed under: Babesiosis, Bartonella, Lyme Disease, co-infections — Tags: , , , , , , , , , , , , , , , , — joethetick @ 11:21 am

By Dr. Jon Sterngold/Special for The Willits News

What are the symptoms of late-stage Lyme disease complex? I use the term ‘complex’ because the spectrum of symptoms are most often caused by the Lyme germ, Borrelia burgdorferi, and other co-infecting pathogenic organisms the ticks carry and transmit. With names such as Babesia, Bartonella, Mycoplasma, and Anaplasma, these pathogens can dramatically contribute to the degree of disease and complexity of diagnosis and treatment in infected individuals. So, as the immune system loses control of these bugs, they spread and cause inflammation, as well as release toxic molecules that cause symptoms and injury to cells and organs.

With so many different possible combinations of infecting organisms and degrees of immune system compromise, the list of potential symptoms is very long. While one person might just have waxing and waning joint pains, another could be totally disabled with neuropathies that interfere with the ability to walk or even to stand. Some become blind from blood clots in the eyes and some are so fatigued that getting out of bed each day might not be possible. Many are plagued with the dreaded “brain fog” and some develop what appear to be well-known psychiatric diseases, such as bipolar disorder and severe depression. But, these patients need antibiotic treatment as much or more than anti-depressants and other psych meds.

Many patients develop severe pain syndromes involving the back and legs, though involvement can be anywhere in the body. Some patients lose intellectual ability, hearing, the ability to sense heat from cold, and coordinated movements. Most develop insomnia, and many get disabling pain in their feet. Fevers, chills, sweats, dry cough, and body aches can make it seem that some sort of “chronic flu” is going on.

Lyme disease can cause life-threatening cardiac abnormalities. And the list goes on.

Some patients have only several symptoms and some have scores. It is no wonder non-Lyme literate physicians either roll their eyes at the prospect of taking care of a Lyme patient or simply refuse to believe this constellation of symptoms is an active and treatable infectious disease. It is so much easier to believe these patients have psychiatric disease (”it’s all in your head”-type illness) or suffer the aches and pains of aging and a low pain threshold (whiners). It makes the doctor’s life so much easier. Just say no. And believe me, as I said before, I would not relish the notion of taking care of a patient with as complex a disease as my own.

And it’s not even that simple. We now know that in addition to the major germ types listed above, there are dozens to hundreds of genetic variations of these organisms. This introduces a mind-boggling level of diagnostic complexity. Physicians faced with a bad disease, and complex long-term, sometimes dangerous treatment, need as much diagnostic data as possible to justify a treatment plan. But testing for these pathogens is almost a lost cause to date.

There are only a few tests for these bugs, and they miss most of the genetic variants. The tests are very meaningful and helpful when positive, but meaningless when negative. We simply cannot “rule out” an infection with a negative test. Physicians who believe otherwise are wrong, if not downright negligent.

But wait, there’s more!

It’s not just the bugs that determine our illness. Our unique immune system genetics and dysfunction play a large part creating the spectrum of symptoms we develop. It has been found that some genetic types tend to develop more severe disease than others, including subtypes that cannot get well. Some are more prone to creating antibodies that make us ill by attacking our own tissue and some have impaired ability to break down and excrete bacterial toxins. These are some of the reasons that one person’s Lyme disease doesn’t look another’s and why we need Lyme experts to manage sick patients.

ABOUT THE AUTHOR: Jon Sterngold, MD, is a Willits resident and physician

November 6, 2009

Bacterial antibiotic resistance genes discovered

Filed under: Lyme Disease, Lyme Disease News, Uncategorized — Tags: , , , , , , , , , — joethetick @ 6:37 pm

Antibacterial soap, hand sanitizer and antibiotics are all substances that we use in an attempt to kill bacteria that might make us sick.Whether we are concerned about getting strep throat, bacterial meningitis or something else, these prevention methods can offer protection.

However, some bacteria, such as those that cause Staph and MRSA infections, are becoming increasingly resistant to antibiotics. Since the 1930s, researchers have been aware that bacteria may be able to resist treatment because they can morph into the L-form, or bacteria lacking cell walls.

Until the 1980s, not much else could be known about the L-form, but now, researchers at the Bloomberg School of Public Health have used a wide variety of modern molecular tools to learn more about the origin and biological functions of the L-form bacteria.

Ying Zhang, a professor of molecular microbiology and immunology at Bloomberg, is the senior author of the study, which was published in PLoS ONE last month.

Not all bacteria can transform into the L-form, but those that can include Bacillus anthracis (anthrax), Treponema pallidum (syphilis), Mycobacterium tuberculosis (tuberculosis), Heliobacter pylori (stomach ulcers and cancer), Borrelia burgdorferi (Lyme disease) and Escherichia coli (food poisoning). Zhang’s team used E. coli to create a culture of L-form bacteria.

Although it had been difficult to culture L-form bacteria before, Zhang and his team created a new method that more closely simulated the in vivo conditions in which these bacteria form.

“The presence of antibiotic stress is cell wall inhibiting, like penicillin,” Zhang said. To prevent the cells from bursting because of this increased stress, Zhang’s team added sucrose to the cell media.
This culture represented the mechanism that occurs in the body. “L forms are formed in response to stress,” Zhang said. “They have a different mode of survival and replication from classical bacteria.” The cell wall-deficient bacteria cluster together in the shape of a fried egg rather than the smooth, homogeneous appearance of wild-type bacteria cultures.

Not only are L-form bacteria difficult to culture and therefore study, but this “fried egg” cluster is part of what makes the L-form bacteria resistant to antibiotics, in addition to the fact that they do not have cell walls for commonly used antibiotics to disintegrate.

Once Zhang and his team were able to successfully culture L-form E. coli, they screened for and identified mutants that fail to grow at the L-form. From these mutants, they were able to discover a series of genes that were linked with the inability to grow in the L-form.

“These fall into four to five different categories involving extracellular matrix synthesis, membrane proteins, membrane biogenesis, DNA repair as well as iron metabolism and energy metabolism,” Zhang said.

Their identification of these genes and their effect on L-form bacterial expression is a resounding discovery because it was impossible to do before, what with the difficulty of culturing the L-forms of various bacteria. Zhang noted, however, that although his team managed to create and study a culture of L-form bacteria, their study cannot be universal.

“What we can culture is only a small percentage – probably less than 1 percent – of all bacteria on earth,” Zhang said.
“They exist in nature and grow easily, but we’re limited to what we can grow and the form of bacteria that can grow. Bacteria can grow a variety of different forms even for the same species, and can change forms under different conditions. L-forms are one example of changing under antibiotic stress.”

These L-forms of various bacteria may be the underlying reason for chronic resistant and recurring diseases, such as sarcoidosis, various forms of inflammatory bowel diseases and rheumatoid arthritis. Zhang is confident that there will be many practical applications of this discovery.

“It is possible, with our discovery of the L-form genes to develop new antibiotics and more effective ones that can be used with current ones as well as new vaccines to . . . allow these forms to be eliminated by the immune system,” he said.

jhunewsletter.com
By Aleena Lakhanpal

October 29, 2009

Distribution of Antibodies Reactive to Borrelia lonestari and Borrelia burgdorferi in White-Tailed Deer (Odocoileus virginianus) Populations in the Eastern United States

Filed under: Lyme Disease — Tags: , , , , , , , , , , , , — joethetick @ 9:40 am

Southern tick-associated rash illness is a Lyme-like syndrome that occurs in the southern states.

Borrelia lonestari, which has been suggested as a possible causative agent of southern tick-associated rash illness, naturally infects white-tailed deer (WTD; Odocoileus virginianus) and is transmitted by the lone star tick (Amblyomma americanum). To better understand the prevalence and distribution of Borrelia exposure among WTD, we tested WTD from 21 eastern states for antibodies reactive to B. lonestari using an indirect immunofluorescent antibody assay and Borrelia burgdorferi using the IDEXX SNAP® 4Dx® test. A total of 107/714 (15%) had antibodies reactive to B. lonestari, and prevalence of antibodies was higher in deer from southern states (17.5%) than in deer from northern states (9.2%). Using the SNAP 4DX test, we found that 73/723 (10%) were positive for B. burgdorferi, and significantly more northern deer (23.9%) were positive compared with southern deer (3.8%). Our data demonstrate that WTD are exposed to both Borrelia species, but antibody prevalence for exposure to the two species differs regionally and distributions correlate with the presence of Ixodes scapularis and A. americanum ticks.

Jessica H. Murdock, Michael J. Yabsley, Susan E. Little, Ramaswamy Chandrashekar, Thomas P. O’Connor, Joe N. Caudell, Jane E. Huffman, Julia A. Langenberg, Simon Hollamby.

September 3, 2009

Using Lyme Disease As A Model, MU Researchers Find Inflammatory Disease Treatments Will Improve Through The Use Of Lipidomics

Filed under: Lyme Disease, Lyme Disease News — Tags: , , , , , , , , , , , — joethetick @ 5:46 pm

According to the National Center for Chronic Disease Prevention and Health Promotion, 46 million Americans have arthritis. Many of these people take over-the-counter anti-inflammatory medications that block production of certain molecules, known as bioactive lipids, to reduce pain and swelling. Yet, the role of these lipids is not yet understood completely, and medications may have adverse side effects. Recently, University of Missouri researchers completed the first comprehensive analysis of bioactive lipids in an inflammatory response triggered by the Lyme disease agent, Borrelia burgdorferi. This analysis could shed light on the role bioactive lipids play in inflammatory diseases.

“Many diseases, such as arthritis, cardiovascular disease and diabetes are associated with chronic inflammation,” said Charles Brown, associate professor of veterinary pathobiology in the MU College of Veterinary Medicine. “The first step in finding an effective treatment is to understand the basics of an inflammatory response, including the role of bioactive lipids. Understanding how bioactive lipids regulate the disease processes will lead to the development of drugs that have more specific targets and less adverse side effects.”

In the study, researchers investigated the role of certain bioactive lipids in mice infected with Borrelia burgdorferi, the bacteria responsible for Lyme disease. Eicosanoids, which are bioactive lipids that play an important role in inflammatory disease, were extracted from mice that displayed symptoms of Lyme arthritis and from mice who showed no symptoms. The researchers found differences in the amounts of specific eicosanoids in the samples, which correlated with the severity of arthritis in the mice.

“The process of inflammation is not a passive event, but instead is a coordinated, orderly process actively signaled by specific protein and lipid molecules,” Brown said. “Previous studies investigating eicosanoids have focused on singular pathways or phases of the inflammatory response. These studies provided an incomplete picture and gave the impression that some bioactive lipids function in isolation. In our study, we were able to measure virtually all of the known eicosanoids at the same time and examine a more complete picture of the inflammatory response.”

The findings from this study also could translate into a diagnostic tool for assessing individual patients, assist with the development of more disease-specific therapies, and facilitate the progress of individualized medicine, resulting in more effective treatments for inflammatory diseases with fewer side effects.

Lyme arthritis occurs in 60 to 80 percent of individuals not treated with antibiotics at the time of their infection, and patients are typically given anti-inflammatory drugs to treat their pain and swelling. Arthritis in mice caused by Lyme disease is a good model for how bioactive lipids regulate the process of inflammation, because researchers can observe the process from start to finish, Brown said.

The study, “Lipidomic Analysis of Dynamic Eicosaniod Responses During the Induction and Resolution of Lyme Arthritis,” was published in the June issue of The Journal of Biological Chemistry. It was co-authored by Brown; Victoria Blaho, post doctoral researcher in the MU College of Veterinary Medicine; Matthew Buczynski, researcher at the University of California; and Edward Dennis, researcher at the University of California.

Source:
Kelsey Jackson
University of Missouri-Columbia

September 1, 2009

Inflammatory Disease Treatments Will Improve Through the Use of Lipidomics

Filed under: Lyme Disease, Lyme Disease News, Lyme Disease Research — Tags: , , , , , , , , , , , , — joethetick @ 9:00 pm

September 1, 2009 (EurekAlert) – According to the National Center for Chronic Disease Prevention and Health Promotion, 46 million Americans have arthritis. Many of these people take over-the-counter anti-inflammatory medications that block production of certain molecules, known as bioactive lipids, to reduce pain and swelling. Yet, the role of these lipids is not yet understood completely, and medications may have adverse side effects. Recently, University of Missouri researchers completed the first comprehensive analysis of bioactive lipids in an inflammatory response triggered by the Lyme Disease agent, Borrelia burgdorferi. This analysis could shed light on the role bioactive lipids play in inflammatory diseases.
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July 28, 2009

Using Satellites To Study Lyme Disease

Filed under: Lyme Disease, Lyme Disease News, Lyme Disease Research — Tags: , , , , , , , , , , , , , — joethetick @ 7:56 am

Six University of Alabama at Birmingham (UAB) students and two students from other universities are using satellite imagery to identify possible habitats in Alabama for the black-legged tick that carries and transmits Lyme disease.

The students are interns with the NASA-Marshall Space Flight Center DEVELOP Program. DEVELOP is a competitive internship in which students work with NASA and partner-agency scientists to carry out innovative research projects.

The eight students are working in UAB’s Laboratory for Global Health Observation (LGHO) using data from the NASA Advanced Spaceborne Thermal Emission and Reflection Radiometer (ASTER) sensor on board the Terra satellite, as well as DigitalGlobe QuickBird satellite technology. The technology enables the team to identify the environmental factors in Alabama, specifically the Birmingham metro area, necessary for Lyme disease to occur, said UAB senior Nathan Renneboog, 21, the Marshall DEVELOP team leader. The interns work with an adviser, Senior Research Scientist Jeffrey C. Luvall with the NASA Marshall Space Flight Center.

Along with the satellite remote sensing technology, the students are using geographic information systems (GIS) software to generate representations of Alabama in colorful, digital maps on their computer screens. The maps’ color patterns detail conditions on the ground such as soil moisture and vegetation that support habitats for black-legged ticks, also known as deer ticks. Animals like the White-tailed deer and the White-footed mouse often are carriers of the ticks and the disease. Ticks carrying the disease often breed in heavily wooded areas.

“There has been disagreement among health officials about the degree to which Lyme disease exists in Alabama,” Renneboog said. By identifying these habitats, the students want to confirm that conditions are present in Alabama for the disease, he said.

On Wednesday, July 29, team members will share their study results with local health officials to help raise public awareness of Lyme disease, Renneboog said. On Aug. 4, Renneboog will present the project results to senior executives at NASA headquarters in Washington, D.C.

In addition to Renneboog, a native of Ghent, Belgium, the DEVELOP interns are UAB graduate students Lili Xie of Sichuan, China; Kathryn Roa of Davao, Philippines; Stephen Firsing III of Princeton, N.J.; Shveta Setia of Chandigarh, India; and Ret. Lt. Col. Marilyn McAllister of Athens. The team also includes Boston University student Emily Capilouto of Birmingham and LSU student Kyle Levy of Zachary, La.

What is Lyme Disease?

Lyme disease is caused by bacteria called Borrelia burgdorferi. Ticks can transmit the bacteria to people and animals when they bite skin. Symptoms often include a circular skin rash that appears three to 30 days after the tick bite, fever, chills, fatigue, muscle and joint aches and swollen lymph nodes. If left untreated, the disease can spread to other parts of the body. If diagnosed early, however, Lyme disease can be treated with antibiotics, experts say.

About the UAB Laboratory for Global Health Observation

The UAB Laboratory for Global Health Observation (LGHO) is the first satellite remote sensing laboratory in North America with a primary focus on medical and health-based research. Through the LGHO, UAB researchers use satellite imagery for anthropological and archaeological research and to track the spread of diseases on the earth and identify areas in which health disparities are occurring. The LGHO also offers courses in satellite remote sensing.

About the NASA DEVELOP Program

DEVELOP is an applied sciences training and development program that engages students to extend NASA science research and results to scientific and public communities. NASA and partner science advisers assist students in conducting scientific research projects and demonstrating outcomes to community leaders. Projects use NASA science research results, measurements and predictions and address the Applied Sciences National Applications. Professional-caliber products are delivered that can assist community decision-making, and students gain the capability to contribute immediately to the science community.

Source
University of Alabama at Birmingham

February 20, 2006

Plaques of Alzheimer’s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete

Filed under: Lyme Disease, Lyme Disease Research — Tags: , , , , , , — joethetick @ 11:28 am

Elsevier Health Journal
Alan B. MacDonald

St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA
Received 20 February 2006; accepted 23 February 2006

Download PDF

Summary Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the
root cause of the rounded structures called plaques in the Alzheimer brain. Rounded ‘‘plaques’ in high density in brain
tissue are emblematic of Alzheimer’s disease (AD). Plaques may be conceptualized as rounded ‘‘pock mark-like’’ areas
of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date
textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the
disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed
in plaques, amyloid is regularly represented by the ‘‘congophilic core’’ structure which is so named because the waxy
amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a
congophilic amyloid core region (these plaques ‘‘cotton wool’’ type plaques, lack a central congophilic core structure).
Furthermore, there is ‘‘plaque diversity’’ in Alzheimer’s; small, medium and large plaques parallel variable cystic
diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core
and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of
ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer’s, is it
possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned
to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis
for Alzheimer’s disease. In the ‘‘anatomy is destiny’’ model, cysts of borrelia are always round. Why then not accept
roundness as a fundamental ‘‘structure determines function’’ argument for the answer to the mystery of why Alzheimer
plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking
two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship.
Parataxis tells us that what appears to be cause and effect in the couplet ‘‘amyloid plaque’’ merely by a proximity
relationship may be ‘‘spurious causality’’ which is a cognitive dead end.

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