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A new study provides evidence for what so many people complain about - that after being treated for Lyme disease with several weeks of antibiotics - they feel that they are not cured, but instead still suffer from Lyme disease. Lyme disease is caused by the bacterium Borrelia burgdorferi, which is transmitted to a person during a tick bite. However, many medical professionals deny that a person can still have Lyme disease after antibiotic treatment, and instead call the lingering symptoms post-treatment Lyme disease syndrome (PTLDS). It is thought that between 10 to 20% of persons treated with antibiotics for Lyme disease have symptoms of PTLDS.

Hah! The Tulane University researchers found that yes, the live bacteria (B. burgdorferi spirochetes) can still be there in different organs of the body even after 28 days of antibiotic treatment. They studied late Lyme disease in both treated (with antibiotics) and untreated rhesus macaques - primates in which Lyme disease has effects similar to humans. Other studies have also found that the Lyme disease bacteria can evade treatment (here and here). From Medical Xpress:

Lyme bacteria survive 28-day course of antibiotics months after infection

Bay Area Lyme Foundation, a leading sponsor of Lyme disease research in the US, today announced results of two papers published in the peer-reviewed journals PLOS ONE and American Journal of Pathology, that seem to support claims of lingering symptoms reported by many patients who have already received antibiotic treatment for the disease. Based on a single, extensive study of Lyme disease designed by Tulane University researchers, the study employed multiple methods to evaluate the presence of Borrelia burgdorferi spirochetes, the bacteria that cause Lyme disease, before and after antibiotic treatment in primates.

The data show that living B. burgdorferi spirochetes were found in ticks that fed upon the primates and in multiple organs after treatment with 28 days of oral doxycycline. The results also indicated that the immune response to the bacteria varied widely in both treated and untreated subjects. "It is apparent from these data that B. burgdorferi bacteria, which have had time to adapt to their host, have the ability to escape immune recognition, tolerate the antibiotic doxycycline and invade vital organs such as the brain and heart," said lead author Monica Embers, PhD, assistant professor of microbiology and immunology at Tulane University School of Medicine.

"In this study, we were able to observe the existence of microscopic disease and low numbers of bacteria, which would be difficult to 'see' in humans but could possibly be the cause of the variable and nonspecific symptoms that are characteristic of post-treatment Lyme disease syndrome. Although current antibiotic regimens may cure most patients who are treated early, if the infection is allowed to progress, the 28-day treatment may be insufficient, based on these findings," Embers said.

The findings also demonstrated: All subjects treated with antibiotics were found to have some level of infection 7 - 12 months post treatment. Despite testing negative by antibody tests for Lyme disease, two of 10 subjects were still infected with Lyme bacteria in heart and bladder. Lyme bacteria which persist are still viable.

To better elucidate previous animal studies demonstrating that some B. burgdorferi bacteria survive antibiotics, the study explored Lyme disease infection in rhesus macaque primates treated with antibiotics and a control group who were also infected but not treated. 

In the study, ticks carrying B. burgdorferi spirochetes fed on ten primates. Four months post infection, half of the primates (five) received the antibiotic doxycycline orally for 28 days at a proportional dose to that used in human treatment...... The results show: Few subjects displayed a rash. Although all subjects were infected, only one of the 10 displayed a rash with central clearing, the classical "bulls-eye" rash. ... Organs may be infected even if antibody tests are negative...... Intact spirochetes were found in three of five treated and four of five untreated subjects based on xenodiagnosis results 12 months after the tick bite.

Immune responses to B. burgdorferi varied greatly posttreatment .... This is significant because it demonstrates that subjects infected with the same strain of B. burgdorferi may have different immune responses to the same antigen. And, because humans, like primates, are genetically diverse, it underscores that testing antibody responses may be inherently unreliable as a singular diagnostic modality for Lyme disease.

Widespread and variable microscopic disease was observed in all infected subjects, despite antibiotic treatment. Compared to uninfected subjects of the same age, infected subjects in this study (treated and untreated) demonstrated inflammation in and around the heart, in skeletal muscles, joints, and the protective sheath that covers the brain, and near peripheral nerves. Rare, but intact B. burgdorferi spirochetes were found in the tissues of both the treated and untreated subjects. In two subjects treated with doxycycline, multiple Lyme bacteria were observed in the brain tissue [Original study.]

Another article was published this month raising the issue of whether Alzheimer's disease is caused by a microbe - which can explain why all the medicines and experimental drugs aimed at treating the "tangles" or amyloid plaques in the brain are not working as a treatment (because that's the wrong approach). The microbe theory of Alzheimer's disease has been around for decades, but only recently is it starting to be taken seriously. Some of the microbes found in patients with Alzheimer's disease (from analyses of both normal brains and Alzheimer patient brains after death): fungi, Borrelia burgdorferi (Lyme disease), herpes simplex virus Type 1 (HSV1), and Chlamydia pneumoniae.

The general hypotheses seem to be that Alzheimer’s disease is caused by infection, but it isn't linked to any one pathogenic microbe.  Instead, the evidence seems to support that "following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation". So the microbes act as "triggers" for Alzheimer's disease - the microbes get into the brain, and immune responses somehow eventually result in the amyloid plaques and Alzheimer's disease. From The Scientist:

Do Microbes Trigger Alzheimer’s Disease?

In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease. Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.

Allen had recently proposed a novel role for biofilms—colonies of bacteria that adhere to surfaces and are largely resistant to immune attack or antibiotics—in eczema....  Allen knew of recent work showing that Lyme spirochetes form biofilms, which led him to wonder if biofilms might also play a role in Alzheimer’s disease. When Allen stained for biofilms in brains from deceased Alzheimer’s patients, he found them in the same hippocampal locations as amyloid plaquesToll-like receptor 2 (TLR2), a key player in innate immunity, was also present in the same region of the Alzheimer’s brains but not in the controls. He hypothesizes that TLR2 is activated by the presence of bacteria, but is locked out by the biofilm and damages the surrounding tissue instead.

Spirochetes, common members of the oral microbiome, belong to a small set of microbes that cross the blood-brain barrier when they’re circulating in the blood, as they are during active Lyme infections or after oral surgery. However, the bacteria are so slow to divide that it can take decades to grow a biofilm. This time line is consistent with Alzheimer’s being a disease of old age, Allen reasons, and is corroborated by syphilis cases in which the neuroinvasive effects of spirochetes might appear as long as 50 years after primary infection.

Allen’s work contributes to the revival of a long-standing hypothesis concerning the development of Alzheimer’s. For 30 years, a handful of researchers have been pursuing the idea that pathogenic microbes may serve as triggers for the disease’s neuropathology..... In light of continued failures to develop effective drugs, some researchers, such as Harvard neurobiologist Rudolph Tanzi, think it’s high time that more effort and funding go into alternative theories of the disease. “Any hypothesis about Alzheimer’s disease must include amyloid plaques, tangles, inflammation—and, I believe, infection.”

Herpes simplex virus type 1 (HSV1) can acutely infect the brain and cause a rare but very serious encephalitis. In the late 1980s, University of Manchester molecular virologist Ruth Itzhaki noticed that the areas of the brain affected in HSV1 patients were the same as those damaged in patients with Alzheimer’s disease. Knowing that herpes can lie latent in the body for long periods of time, she began to wonder if there was a causal connection between the infection and the neurodegenerative disorder.

Around the same time, neuropathologist Miklossy, then at the University of Lausanne in Switzerland, was detailing the brain damage caused by spirochetes—both in neurosyphilis and neuroborrelia, a syndrome caused by Lyme bacteria. She happened upon a head trauma case with evidence of bacterial invasion and plaque formation, and turned her attention to Alzheimer’s. She isolated spirochetes from brain tissue in 14 Alzheimer’s patients but detected none in 13 age-matched controls. In addition, monoclonal antibodies that target the amyloid precursor protein (APP)—which, when cleaved, forms amyloid-β—cross-reacted with the spirochete species found, suggesting the bacteria might be the source of the protein.

Meanwhile, in the U.S., a third line of evidence linking Alzheimer’s to microbial infection began to emerge. While serving on a fraud investigation committee, Alan Hudson, a microbiologist then at MCP-Hahnemann School of Medicine in Philadelphia, met Brian Balin.... Soon, Balin began to send Hudson Alzheimer’s brain tissue to test for intracellular bacteria in the Chlamydia genus. Some samples tested positive for C. pneumoniae: specifically, the bacteria resided in microglia and astrocytes in regions of the brain associated with Alzheimer’s neuropathology, such as the hippocampus and other limbic system areas. Hudson had a second technician repeat the tests before he called Balin to unblind the samples. The negatives were from control brains; the positives all had advanced Alzheimer’s disease. "We were floored,” Hudson says.

Thus, as early as the 1990s, three laboratories in different countries, each studying different organisms, had each implicated human pathogens in the etiology of Alzheimer’s disease. But the suggestion that Alzheimer’s might have some microbial infection component was still well outside of the theoretical mainstream. Last year, Itzhaki, Miklossy, Hudson, and Balin, along with 29 other scientists, published a review in the Journal of Alzheimer’s Disease to lay out the evidence implicating a causal role for microbes in the disease.

The microbe theorists freely admit that their proposed microbial triggers are not the only cause of Alzheimer’s disease. In Itzhaki’s case, some 40 percent of cases are not explained by HSV1 infection. Of course, the idea that Alzheimer’s might be linked to infection isn’t limited to any one pathogen; the hypothesis is simply that, following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation.

 Lyme disease is caused by the bacterium Borrelia burgdorferi and is typically treated with antibiotics. This study may go a long way in explaining why some people do not seem to respond to Lyme disease treatment, and why they continue to feel sick even after prolonged antibiotic therapy. The researchers discussed how, in addition to the familiar spirochete form, B. burgdorferi can transform from spirochetes into round body forms in the presence of various unfavorable environmental conditions, including the presence of antimicrobial agents (antibiotics). And that the different forms respond to different antibiotic treatments!

But now they found that this bacterium has an additional form, which they refer to as biofilm, and which may be resistant to even very aggressive antibiotic (antimicrobial) treatments. They say this is the first study that demonstrates the presence of Borrelia biofilm in infected human skin tissues. From Medical Xpress:

Lyme disease 'Biofilm' eludes antibiotics: report

In many cases, Lyme disease returns after a patient has completed antibiotic treatment, and this finding may help explain why that occurs, the researchers said. University of New Haven researchers determined that Lyme disease-causing Borrelia burgdorferi bacteria produces a biofilm that makes it up to 1,000 times more resistant to antibiotics than other bacteria.

The discovery may lead to new ways to treat Lyme disease, said study author Eva Sapi, head of biology and environmental sciences at the university. "These findings could change the way we think about Lyme disease, especially in patients where it seems to be a persistent disease, despite long-term antibiotic treatment," she said in a news release from the Connecticut-based university.

"This recent finding could help to better understand how Borrelia can survive treatment and ... will provide novel therapeutic targets for chronic Lyme disease, with the hope of eradicating Borrelia in these patients," Sapi added. (original study)

 Borrelia burgdorferi  Credit: CDC

 Another microbe that causes Lyme disease! Lyme disease is the most common tick-borne disease in the northern hemisphere, and it is caused by the bacteria Borrelia burgdorferi. Recently Mayo Clinic researchers found a new bacteria, which they named Borrelia mayonii, in the fluids and tissues of some people diagnosed with Lyme disease in the upper midwestern USA. The symptoms are different from typical Lyme disease: with nausea and vomiting, diffuse rashes (rather than a single bull's-eye rash), and a higher concentration of bacteria in the blood. Same treatment as with the original bacteria , but it may not show up in tests for Lyme disease.

Other researchers say that other Borrelia species found throughout the US and Europe also cause Lyme disease. This may explain why Lyme diseasse sufferers are not always diagnosed with Lyme disease, even though they have it. From Scientific American:

New Cause for Lyme Disease Complicates Already Murky Diagnosis

Tick-borne Lyme disease in the U.S. has long been thought to be caused by a single microbe, a spiral-shaped bacterium called Borrelia burgdorferi. Last week this notion was challenged when a team led by scientists at the Mayo Clinic discovered that Lyme could be caused, albeit rarely, by a different bacterial species that may incite more serious symptoms ranging from vomiting to neurological issues. Scientists working in the contentious field of Lyme disagree, however, as to what this information means for public health and if these findings are truly the first of their kind. For years, they say, research has pointed to the notion that the spirochete that causes Lyme disease in the U.S. is more heterogeneous than many have acknowledged.

In the new study, recently published in The Lancet Infectious Diseases,Mayo Clinic pathologist and laboratory doctor Bobbi Pritt and her colleagues tested more than 100,500 clinical specimens, such as blood, cerebrospinal fluid and tissue, collected from U.S. patients with suspected Lyme disease between 2003 and 2014. Using a special molecular biology technique called PCR that can identify genetic differences among bacterial strains, they found that six of the samples—collected from patients between 2012 and 2014 in Wisconsin, Minnesota and North Dakota—contained DNA suggestive of a new species. They isolated some of these live bacteria and analyzed parts of their genetic sequence, confirming that the microbe has, in fact, never been documented before. The researchers propose to name the new species Borrelia mayonii

Whereas these findings have been touted as the first evidence that bacteria other than B. burgdorferi can cause Lyme in the U.S., “other Borrelia species have [in the past] been implicated,” says Richard Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies. For example, in 2011 researchers led by Yvette Girard, a medical entomologist at the University of California, Berkeley, found DNA close in sequence to a spirochete called Borrelia bissettii, which has been implicated in Lyme disease in Europe, in three California individuals. Kerry Clark, a tick-borne disease ecologist and epidemiologist at the University of North Florida, and his colleagues also found B. bissettii DNA in an individual from the U.S. Southeast, and they identified the DNA of two other Borrelia species in a handful of Florida and Georgia individuals with Lyme-like symptoms.

Lyme-causing bacteria are complex for another reason: Even within a single species of Borrelia, diversity flourishes. Contrary to what has long been believed, B. burgdorferi can genetically recombine to create different strains that behave dissimilarly inside the human body. Some strains seem more likely to remain in the skin whereas others are more likely to invade the nervous system or heart. Some strains are also more commonly found in certain parts of the country. “When I started out and we identified a tick as having Borrelia burgdorferi, we thought that was the gold standard—aha!—but now we are not thinking that way,” says Robert Lane, a medical entomologist at the University of California at Berkeley. “We have to go within the species itself and break it down further, according to strains or genotypes or alleles. As we learn more, it gets more complicated over time to disentangle the transmission cycles in nature and also what’s going on in the human body after exposure to a given spirochete.”

Could some of these differences explain why Lyme patients report diverse symptoms and treatment outcomes? Weigang Qiu, a biologist who studiesBorrelia genetics at Hunter College in New York City, says no one yet knows. “This is the most important question, but we haven’t found a definitive answer yet,” he says. B. mayonii, though, seems to cause strange and serious symptoms: Some patients experienced nausea and vomiting and had diffuse and spotty rashes that were drastically different from the typical Lyme bulls-eye rash. Half displayed neurological problems and one third were hospitalized.

All these scientific challenges could help explain why there are so many rifts within the Lyme research community. The organism is difficult to study and genetically diverse, and its ecology—the complicated and intricate dance that takes place between the ticks, their spirochetes and their numerous animal and human hosts—is immensely difficult to track and understand. “To me, the underlying biology that paves the way for controversy and vastly different perspectives is all a function of the amazing complexity and sophistication of Borrelia,” Ostfeld says. Adding to the problem, scientists bring to the field different backgrounds, methodologies, standards of evidence and preconceptions.
 
The new bacterium could complicate the diagnosis of Lyme, too, which has long been a contentious issue. Even with B. burgdorferi–caused Lyme, government-recommended diagnostic tests do not typically work in the first four weeks of infection; blood antibody levels are too low. (Three of the six patients who had B. mayonii in the Mayo Clinic study would have failed the standard Lyme tests based on their antibody results.)

Because of these difficulties, physicians diagnosing Lyme in its early stages are supposed to rely entirely on clinical cues such as the characteristic bulls-eye rash, fever, aches and fatigue. But what if a patient is vomiting and has a spotty rash? “People may not think of a tick-borne disease with that,” Aucott says, so cases of B. mayonii may go undiagnosed and untreated. (B. burgdorferi–caused Lyme disease, he adds, does not always cause a bulls-eye rash either.) Pritt and her colleagues recommend that physicians use their PCR (polymerase chain reaction) test to diagnose B. mayonii early on, as these bacteria, unlike B. burgdorferi, proliferate readily in blood. But Aucott points out that these tests require physicians to send samples to the Mayo Clinic, and “that just may not happen.”

A cluster of Borrelia burgdorferi bacteria, which Lyme disease. Humans catch it when bitten by ticks. These bacteria belong to a group called spirochetes, which resemble coiled springs.  A cluster of Borrelia burgdorferi bacteria, which causes Lyme disease.  Credit: CDC/ Claudia Molins photo: Janice Haney Carr

 Adult deer tick, Ixodes scapularisCredit:  Scott Bauer/USDA

 I recently posted on ways the number of  ticks can be reduced in a backyard. Now an article on vaccines being developed to battle tick borne diseases, especially Lyme disease. However, the bad news is that ticks now transmit 16 diseases in the US (including anaplasmosis, babesiosis, ehrlichiosis), while vaccines typically only focus on one disease at a time. Tick borne diseases are on the rise throughout the world. We all know about Lyme disease (which is also a problem in Europe, China, and Mongolia), but in parts of Africa, the Middle East, Asia and southern Europe, ticks can spread Crimean–Congo haemorrhagic fever, which is fatal 40% of the time! And while some researchers are focusing on human vaccines, some are focusing on vaccines for mice. Big problem: would we really be able to give the vaccine to enough mice to make a difference? I really like the idea of a vaccine that hampers the ability of ticks to feed on humans. From Nature:

The new war on Lyme and other tick-borne diseases

Williams is testing whether vaccinating mice against Borrelia burgdorferi, the bacterium that causes Lyme disease in the United States, can reduce the proportion of ticks that are infected. ....Borrelia burgdorferi infects an estimated 329,000 people in the United States each year, according to the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia. And although most people who get prompt treatment recover quickly — Williams has had Lyme three times — up to one in five develops long-term and potentially life-threatening symptoms, including heart, vision or memory problems, or debilitating joint pain.

Williams's approach is one of several strategies being tested in an attempt to thwart the spread of tick-borne diseases. Some, like the mouse vaccine, interrupt the pathogen's ecological circuitry by targeting the wild animals that pass along and amplify the disease. Others, such as efforts to revive a human Lyme vaccine, aim to protect people from infection directly. A more radical approach could hamper the ability of ticks to bite humans or animals, potentially protecting against dozens of illnesses spreading across the United States, Europe, Africa and Asia.

That the field needs creative solutions is clear. Many long-recommended interventions, such as pesticide application or controlling populations of deer, which are an important host for adult ticks, have had mixed success in scientific studies. Even the time-honoured protective strategies that most people use are not evidence-based. “We tell people to wear repellents, to do tick checks and to shower if they've been in the field, but there's very little data to show that these things reduce human illness,” explains Ben Beard, chief of the CDC's bacterial-diseases branch in the division of vector-borne diseases.

The plan is unconventional, because most Lyme-control measures focus on white-tailed deer (Odocoileus virginianus), which have exploded in number in the United States over the past century as young forests have become increasingly fragmented by human development and large predators have been all but eradicated. Adult blacklegged ticks (Ixodes scapularis) typically feed and mate on deer, so many scientists have argued that the only way to get rid of Lyme is to get rid of the deer. But such efforts have had “an incredibly spotty record”, says Richard Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies in Millbrook, New York, who has been studying tick-borne diseases for decades.

Ostfeld and others contend that mice are a major driver for both the tick problem and the disease problem. Mice, like deer, flourish in fragmented woodlands — in part because predators such as foxes and opossums get displaced. Ticks then thrive on the rodents, which are poor groomers. Studies suggest that larval ticks have a 50% chance of surviving when they feed on mice, but only a 3.5% chance on opossums2.

And mice are typically where ticks pick up B. burgdorferi. Most mice in Lyme-endemic areas get infected with the bacterium at a young age and, for reasons that are not completely clear, they are particularly good at transmitting it to other ticks. Almost all young ticks that feed on white-footed mice become infected, compared with a mere 1% of ticks that feed on deer. Interrupting the tick–mouse infection cycle, says Ostfeld, could make ticks a lot less dangerous.... The bait-based vaccine is also attractive because it is less ecologically destructive than other strategies — it does not kill animals or even ticks, just the pathogens.

Other scientists argue for more a direct means of protecting people against Lyme, ideally with a human vaccine. ....product called LYMErix, manufactured by UK-based pharmaceutical company SmithKline Beecham (now GlaxoSmithKline), was approved by the US Food and Drug Administration in 1998. It reduced the risk of Lyme caused by US strains of Borrelia by 76% in clinical trials4. But it faced problems from the start....The company voluntarily shelved LYMErix in 2002. Plotkin maintains that this was a mistake. “The vaccine was safe,” he says.

Now, a new and potentially improved vaccine has completed safety trials5. Developed by researchers at Stony Brook University and Brookhaven National Laboratory in New York, and licensed to Baxter Innovations in Vienna... it protects against many Borrelia species known to cause Lyme in humans, including those that affect people in Europe....Richard Marconi, a microbiologist and vaccinologist at Virginia Commonwealth University in Richmond, says that he and his colleagues are working on an even better vaccine.

Mouse vaccines would not raise such concerns, but some researchers, including Plotkin, are sceptical about whether they could dose enough mice to reduce Lyme rates. And both vaccine approaches are limited because they combat only one tick-borne disease, when more than a dozen others are spreading throughout the world (see 'Reality bites').

There is one strategy that could conquer them all, and it involves turning one of the tick's most ingenious tools — its saliva — against it. When a tick bites a host, molecules in its saliva help it to evade detection and start to feed by blocking pain, inflammation and immune signals. If a vaccine could raise an immune response to key salivary proteins, it could make tick bites more noticeable or block the tick's ability to feed. Ostfeld himself is a proof-of-concept for this approach. He has been bitten more than 100 times, and his body now reacts to tick saliva. “I realize when a tick is biting me because I get a burning sensation. It's pretty intense,” he explains. 

A European Commission-funded consortium called ANTIDotE (Anti-tick Vaccines to Prevent Tick-borne Diseases in Europe) is characterizing the tick salivary proteins that could be targeted to thwart feeding. “We think that an anti-tick vaccine could be immensely useful in protecting both humans and animals,” says Hein Sprong, an ANTIDotE leader at the National Institute for Public Health and the Environment in Bilthoven, the Netherlands. US Biologic also plans to develop a bait-based vaccine for mice that could thwart tick feeding, thereby protecting against multiple diseases. That could reduce overall tick numbers, too, because it would make it difficult for larval ticks to get the meals that they need to survive into adulthood and reproduce.

But these approaches are hardly around the corner. Part of the problem, scientists say, is that funding is scarce. The stereotype of Lyme and other US tick-borne diseases as primarily 'yuppie' illnesses does not help;... Until an all-encompassing solution becomes available, controlling tick-borne diseases will probably require an array of smaller-scale approaches that attack the problem, bit by bit, on a number of levels. 

 Deer can harbor many engorged ticks behind their ears; the ticks drop off in areas where the deer pass through or rest. Credit: Peter Priolo

 Nice article about ticks, tickborne diseases (of which Lyme disease is one), and possible strategies for coping - whether getting rid of ticks in your yard, or minimizing risk. The only thing I disagreed with is that the author gives the time for transmission of a tick borne disease as needing over 24 hours of the tick being attached (this number is frequently given by authorities). Others disagree (as do I based on experience), and a recent article on transmission time after attachment stated that in animal research, transmission can occur in <16 hours. Some human studies also found transmission times of less than 24 hours (and as little as 6 hours of tick attachment), but so far the minimum attachment time for transmission of infection has never been established. Read the complete article for more pet and tick advice. From Mother Earth News:

How to Get Rid of Ticks and Prevent Lyme Disease 

About 300,000 people are diagnosed with Lyme disease every year, according to new estimates from the Centers for Disease Control and Prevention (CDC). Lyme disease is caused by bacteria that multiply in the bodies of ticks, people and animals, including mice, deer and dogs....  the tiny blacklegged deer tick, which is the most common transmitter of Lyme disease.

These deer ticks pick up Lyme bacteria (Borrelia burgdorferi) when they feed on the blood of infected mice, chipmunks and other hosts. Infected ticks in both the nymphal and adult life stages can then transfer the Lyme bacteria to humans if they latch on for a meal and feed for approximately 36 hours or more. Lyme disease is highly treatable when it’s detected early, but devastating when the infection goes unnoticed for more than a few months.

Let Poultry Help with Tick Prevention  Leafy wooded areas and grassy meadows are the preferred habitats for blacklegged deer ticks and American dog ticks, which both spend their larval stage in leaf litter, their nymphal stage on small animals, and their adult stage in tall grass or other shrubby vegetation. People have learned how to get rid of ticks by keeping foraging chickens and guinea fowl on their property. In April 2015, we launched the MOTHER EARTH NEWS Chickens and Ticks Survey, and responses revealed that: 71 percent had an existing tick problem before they got poultry, 78 percent kept poultry that helped control or eliminate ticks within the birds’ feeding range, 46 percent experienced a drop in tick populations within a month after getting poultry; 45 percent saw good control after several months to a year.Many respondents noted that small bantam chickens and game hens can get into tight spots where larger birds can’t fit, resulting in better tick control....

Permethrin-Treated Clothes and ‘Tick Tubes’  If you live in one of the 13 states where Lyme disease risk is highest, learning how to get rid of ticks should be a top priority. You might want to consider using permethrin, a non-organic pesticide that repels and kills ticks. Permethrin is more potent and persistent than the organic materials we usually recommend. We suggest using a formula designed to be applied to clothing rather than misters, sprayers, foggers or other permethrin products. Clothing products that are pre-treated with permethrin are available, or you can buy permethrin with instructions for how to use it to treat your clothes. Take care to not expose kids to this pesticide...The EPA also classified permethrin as “likely to be carcinogenic to humans,” so weigh the risk of infrequent exposure to the risk of Lyme disease in your area.

You might also consider permethrin-infused “tick tubes,” which are designed to kill ticks on white-footed mice as well as chipmunks and rats, the main animals from which ticks become infected with Lyme. The tick tubes offer nesting materials impregnated with the pesticide to such critters. The animals then take the material back to their nests, where it kills any ticks that may have latched on to the adults and their young. The small amount of permethrin used in tick tubes is not water-soluble, so it’s not likely to end up anywhere but in a nest. Sold commercially as Damminix Tick Tubes, these devices are easy to make yourself....

Herbal Tick Repellents   Many of our survey respondents reported that they apply veterinary-prescribed tick preventatives on their dogs and cats, but would prefer more organic repellents. Two plant-based aromatics — sweet-scented “rose” geranium (Pelargonium graveolens) essential oil and eastern red cedar (Juniperus virginiana; also known as “red cedarwood”) essential oil — were repeatedly recommended by readers who use them as spray-on repellents for pets and family members alike....Both geranium essential oil and eastern red cedar essential oil have proven to be successful repellents against ticks in various life stages, according to the Journal of Agricultural and Food Chemistry and the Journal of Medical Entomology, respectively.

Using full-strength essential oil can injure human skin and overwhelm pets’ sensitive noses, so follow this simple recipe when making a liquid anti-tick spray: In an 8-ounce spray bottle, combine 10 to 20 drops of rose geranium or eastern red cedar essential oil with 1 teaspoon of vodka or rubbing alcohol. Fill the rest of the bottle with water and shake to combine. The spray can be applied to your skin or clothing....

More Tick Prevention Tricks Fencing out deer, the primary host of adult Lyme-infected ticks, can help prevent ticks from reaching your land. Low-cost, plastic-mesh deer fencing is available online and at farm stores. Ticks rarely inhabit lawns that are mowed regularly. Raking up leaves and composting them deprives overwintering ticks of shelter.

When hiking where tick populations are high, stay on the trails and dress defensively — pull your socks up over your pants. When only shorts will do, some people cut off the ankle sections of old socks, spray them with a repellent, and wear the tubes around their calves like tick-deterring leg warmers.

A study published in Experimental and Applied Acarology found that spraying outdoor areas with Safer-brand organic insecticidal soap in spring, when blacklegged deer tick nymphs are active, can provide treatment that is equally as effective as spraying with the insecticide chlorpyrifos.

After you’ve been outdoors, check your dogs for any ticks that may have latched on, and then make your way to a hot, soapy shower followed by a careful body check. You can kill any ticks that have attached to your clothing by immediately putting your clothes into the dryer for 15 minutes on the hottest setting, and then washing them. Most ticks are sensitive to dry heat, but may survive even the hottest wash.

Poultry are tick hunters.
Photo by Getty Images/Catherine MacBride

I know of a number of people in NY and NJ who have been struggling for years with persistent Lyme disease. So this research with the possibility of treatments that actually work is fantastic. And it gives support to all those people who say they still have Lyme disease after antibiotic treatment, but the medical establishment says they're wrong -  that it's all their mind or due to something else. Yes, they still have Lyme disease from persister cells that avoided the antibiotic treatment! Persister cells are drug-tolerant,dormant variants of Borrelia burgdorferi  (the bacterium that causes Lyme disease). And perhaps pulse-dosing antibiotics may work to get rid of the persister cells. The antibiotic they successfully used in the research is ceftriaxone (a cephalosporin antibiotic) - but only in cultures grown in a lab. Further research is needed. From Science Daily:

Researchers' discovery may explain difficulty in treating Lyme disease

North­eastern Uni­ver­sity researchers have found that the bac­terium that causes Lyme dis­ease forms dor­mant per­sister cells, which are known to evade antibi­otics. This sig­nif­i­cant finding, they said, could help explain why it's so dif­fi­cult to treat the infec­tion in some patients.

In other chronic infec­tions, Lewis' lab has tracked the resis­tance to antibi­otic therapy to the pres­ence of per­sister cells--which are drug-tolerant, dor­mant vari­ants of reg­ular cells. These per­sister cells are exactly what they've iden­ti­fied here in Bor­relia burgdor­feri, the bac­terium that causes Lyme disease.The researchers have also reported two approaches--one of them quite promising--to erad­i­cate Lyme dis­ease, as well as poten­tially other nasty infections.

Lyme dis­ease affects 300,000 people annu­ally in the U.S., according to the Cen­ters for Dis­ease Con­trol and Pre­ven­tion, and is trans­mitted to people via bites from infected black­legged ticks. If caught early, patients treated with antibi­otics usu­ally recover quickly. How­ever, about 10 to 20 per­cent of patients, par­tic­u­larly those diag­nosed later, who have received antibi­otic treat­ment may have per­sis­tent and recur­ring symp­toms including arthritis, muscle pain, fatigue, and neu­ro­log­ical prob­lems. These patients are diag­nosed with Post-treatment Lyme Dis­ease Syndrome.

In addi­tion to iden­ti­fying the pres­ence of these per­sister cells, Lewis' team also pre­sented two methods for wiping out the infection--both of which were suc­cessful in lab tests. One involved an anti-cancer agent called Mit­o­mycin C, which com­pletely erad­i­cated all cul­tures of the bac­terium in one fell swoop. How­ever, Lewis stressed that, given Mit­o­mycin C's tox­i­city, it isn't a rec­om­mended option for treating Lyme dis­ease, though his team's find­ings are useful to helping to better under­stand the disease.

The second approach, which Lewis noted is much more prac­tical, involved pulse-dosing an antibi­otic to elim­i­nate per­sis­ters. The researchers intro­duced the antibi­otic a first time, which killed the growing cells but not the dor­mant per­sis­ters. But once the antibi­otic washed away, the per­sis­ters woke up, and before they had time to restore their pop­u­la­tion the researchers hit them with the antibi­otic again. Four rounds of antibi­otic treat­ments com­pletely erad­i­cated the per­sis­ters in a test tube.

"This is the first time, we think, that pulse-dosing has been pub­lished as a method for erad­i­cating the pop­u­la­tion of a pathogen with antibi­otics that don't kill dor­mant cells," Lewis said. "The trick to doing this is to allow the dor­mant cells to wake up.

This is part 2 of today's post. This past week I came across two amazing and very different stories, but in both Lyme disease appears. So read with an open mind - because they may or may not work out. But I will say that living in the NY metro area, tick diseases are a big deal, and we all know people who have gotten diseases from ticks. Most get successfully treated with antibiotics, but then there are those people who are suffering years later with all sorts of symptoms . The following article may be considered speculative by many in raising a Lyme disease and Morgellons disease link, but it is nonetheless very interesting with a famous personality (Joni Mitchell) involved. The mysterious disease has been the subject of much debate, but many doctors and the CDC  think Morgellons disease is actually a delusional infestation or delusions of parasitosis (DOP) - a psychiatric condition in which people falsely believe themselves to be infested. Finally, I give a link to recent research showing a Morgellons disease and Lyme disease link.From MNN:

The mystery surrounding Morgellons disease

Earlier this week, legendary singer Joni Mitchell was rushed to the hospital after fainting at her home in Bel Air, California. While still under observation by doctors, an update provided to fans said the 71-year-old is resting comfortably and that "she continues to improve and get stronger each day." What was not disclosed was the exact illness Mitchell is suffering from, leading to speculation that  Morgellons disease, a health condition she's spoken about in the past, might be responsible. I have this weird, incurable disease that seems like it's from outer space," she told the LA Times in 2010. "Fibers in a variety of colors protrude out of my skin like mushrooms after a rainstorm: they cannot be forensically identified as animal, vegetable or mineral. Morgellons is a slow, unpredictable killer — a terrorist disease: it will blow up one of your organs, leaving you in bed for a year."

If that sounds like something awful that deserves more attention from the medical community, there are others out there suffering from similar symptoms who share your concern. Doctors, however, are split on what exactly Morgellons is, with some believing it is psychosomatic and others believing it's a real unexplained condition, or even possibly a complication related to tick-borne illnesses

 In a 2012 study on Morgellons, researchers at the Centers for Disease Control and Prevention (CDC) defined the disease as "a poorly characterized constellation of symptoms, with the primary manifestations involving the skin." After finding no parasites or mycobacteria, the panel concluded that the symptoms were not caused by an infection or environmental agent, but may be associated with what's termed a "delusional infestation." The skin fibers collected during the study were found to have come from "environmental sources," mainly composed of cotton. In a separate summary, the CDC determined that it would not "be helpful to perform additional testing for infectious diseases as a potential cause."

Researchers involved in studying both tick-borne diseases and Morgellons conducted their own study in 2013 on the mysterious filaments that contradicted the CDC's findings. After collecting fibers from a group of four patients with classic Morgellons symptoms, they exposed the filaments under an electron microscope and discovered them to be "keratin and collagen in composition" and originating from within the epidermis. It's interesting to note that all four patients had also previously tested positive for Borrelia burgdorferi, a causative agent of Lyme disease

 Dr. Anne Louise Oaklander, a neurologist at Massachusetts General Hospital who specializes in itches affecting the body, told the Guardian that whatever Morgellons is, those who have it are experiencing true discomfort.  "In my experience, Morgellons patients are doing the best they can to make sense of symptoms that are real. They're suffering from a chronic itch disorder that's undiagnosed. They have been maltreated by the medical establishment. And you are welcome to quote me on that," she said. 

And last is a Feb 2015 study finding a Morgellons disease and Lyme disease link. From BMC Dermatology: Exploring the association between Morgellons disease and Lyme disease: identification of Borrelia burgdorferi in Morgellons disease patients

Morgellons disease (MD) is a complex skin disorder characterized by ulcerating lesions that have protruding or embedded filaments. Many clinicians refer to this condition as delusional parasitosis or delusional infestation and consider the filaments to be introduced textile fibers. In contrast, recent studies indicate that MD is a true somatic illness associated with tickborne infection, that the filaments are keratin and collagen in composition and that they result from proliferation and activation of keratinocytes and fibroblasts in the skin. Previously, spirochetes have been detected in the dermatological specimens from four MD patients, thus providing evidence of an infectious process.

Our study using multiple detection methods confirms that MD is a true somatic illness associated with Borrelia spirochetes that cause Lyme disease. Further studies are needed to determine the optimal treatment for this spirochete-associated dermopathy.

This past week I came across two amazing and very different stories, but in both Lyme disease appears. So read with an open mind - because they may or may not work out. But I will say that living in the NY metro area, tick diseases are a big deal, and we all know people who have gotten diseases from ticks. Most get successfully treated with antibiotics, but then there are those people who are suffering years later. The first article is by Dr. Christie Wilcox (a freelance science writer and postdoctoral researcher). Do go read the whole article for her fascinating account of venoms. From Digg:

Poison As Medicine: How A Bee Sting Saved My Life

“I moved to California to die.” Ellie Lobel was 27 when she was bitten by a tick and contracted Lyme disease. And she was not yet 45 when she decided to give up fighting for survival. Caused by corkscrew-shaped bacteria called Borrelia burgdorferi, which enter the body through the bite of a tick, Lyme disease is diagnosed in around 300,000 people every year in the United States. It kills almost none of these people, and is by and large curable – if caught in time. If doctors correctly identify the cause of the illness early on, antibiotics can wipe out the bacteria quickly before they spread through the heart, joints and nervous system.

But back in the spring of 1996, Ellie didn’t know to look for the characteristic bull’s-eye rash when she was bitten – she thought it was just a weird spider bite. Then came three months with flu-like symptoms and horrible pains that moved around the body. Ellie was a fit, active woman with three kids, but her body did not know how to handle this new invader. She was incapacitated. “It was all I could do to get my head up off the pillow,” Ellie remembers.

As time wore on, Ellie went to doctor after doctor, each giving her a different diagnosis. Multiple sclerosis. Lupus. Rheumatoid arthritis. Fibromyalgia. None of them realised she was infected with Borrelia until more than a year after she contracted the disease – and by then, it was far too late. Lyme bacteria are exceptionally good at adapting, with some evidence that they may be capable of dodging both the immune system and the arsenal of antibiotics currently available. Borrelia are able to live all over the body, including the brain, leading to neurological symptoms. And even with antibiotic treatment, 10–20 per cent of patients don’t get better right away. There are testimonies of symptoms persisting – sometimes even resurfacing decades after the initial infection – though the exact cause of such post-treatment Lyme disease syndrome is a topic of debate among Lyme scientists.

I just kept doing this treatment and that treatment,” says Ellie. Her condition was constantly worsening....So she packed up everything and moved to California to die. And she almost did. Less than a week after moving, Ellie was attacked by a swarm of Africanised bees....Bees – and some other species in the order Hymenoptera, such as ants and wasps – are armed with a potent sting that many of us are all too aware of. This is their venom, and it’s a mixture of many compounds. Perhaps the most important is a tiny 26-amino-acid peptide called melittin, which constitutes more than half of the venom of honey bees and is found in a number of other bees and wasps. 

“I just went limp. I put my hands up and covered my face because I didn’t want them stinging me in the eyes… The next thing I know, the bees are gone.” When the bees finally dissipated, her caregiver tried to take her to the hospital, but Ellie refused to go... But Ellie didn’t die. Not that day, and not three to four months later...She believes the bees, and their venom, saved her life.

The idea that the same venom toxins that cause harm may also be used to heal is not new. Bee venom has been used as a treatment in East Asia since at least the second century BCE...Despite the wealth of history, the practical application of venoms in modern therapeutics has been minimal....Over the course of the 20th century, suggested venom treatments for a range of diseases have appeared in scientific and medical literature. Venoms have been shown to fight cancer, kill bacteria, and even serve as potent painkillers – though many have only gone as far as animal tests

The more we learn about the venoms that cause such awful damage, the more we realise, medically speaking, how useful they can be. Like the melittin in bee venomMelittin does not only cause pain. In the right doses, it punches holes in cells’ protective membranes, causing the cells to explode. At low doses, melittin associates with the membranes, activating lipid-cutting enzymes that mimic the inflammation caused by heat. But at higher concentrations, and under the right conditions, melittin molecules group together into rings creating large pores in membranes, weakening a cell’s protective barrier and causing the entire cell to swell and pop like a balloon.Because of this, melittin is a potent antimicrobial, fighting off a variety of bacteria and fungi with ease. 

After the attack, Ellie watched the clock, waiting for anaphylaxis to set in, but it didn’t. Instead, three hours later, her body was racked with pains. A scientist by education before Lyme took its toll, Ellie thinks that these weren’t a part of an allergic response, but instead indicated a Jarisch–Herxheimer reaction – her body was being flooded with toxins from dying bacteria. The same kind of thing can happen when a person is cured from a bad case of syphilis. A theory is that certain bacterial species go down swinging, releasing nasty compounds that cause fever, rash and other symptoms. For three days, she was in pain. Then, she wasn’t.“I had been living in this… I call it a brown-out because it’s like you’re walking around in a half-coma all the time with the inflammation of your brain from the Lyme. My brain just came right out of that fog. I thought: I can actually think clearly for the first time in years.”

With a now-clear head, Ellie started wondering what had happened. So she did what anyone else would do: Google it. Disappointingly, her searches turned up very little. But she did find one small 1997 study by scientists at the Rocky Mountain Laboratories in Montana, who’d found that melittin killed Borrelia. Exposing cell cultures to purified melittin, they reported that the compound completely inhibited Borrelia growth. When they looked more closely, they saw that shortly after melittin was added, the bacteria were effectively paralysed, unable to move as their outer membranes were under attack. Soon after, those membranes began to fall apart, killing the bacteria.

Convinced by her experience and the limited research she found, Ellie decided to try apitherapy, the therapeutic use of materials derived from bees...She started on a regimen of ten stings a day, three days a week: Monday, Wednesday, Friday. Three years and several thousand stings later, Ellie seems to have recovered miraculously. Slowly, she has reduced the number of stings and their frequency – just three stings in the past eight months, she tells me (and one of those she tried in response to swelling from a broken bone, rather than Lyme-related symptoms). 

Since the 1997 study, no one had looked further into bee venom as a potential cure for Lyme disease, until Ellie. Ellie now runs a business selling bee-derived beauty products called BeeVinity, inspired after, she says, noticing how good her skin looked as she underwent apitherapy.....In addition, she sends some of the venom she purchases – which, due to the cost of the no-harm extraction method she uses, she says is “more expensive than gold” – to Eva Sapi, Associate Professor of Biology and Environmental Science at the University of New Haven, who studies Lyme disease.

Sapi’s research into the venom’s effects on Lyme bacteria is ongoing and as yet unpublished, though she told me the results from preliminary work done by one of her students look “very promising”. Borrelia bacteria can shift between different forms in the body, which is part of what makes them so hard to kill. Sapi has found that other antibiotics don’t actually kill the bacteria but just push them into another form that is more dormant. As soon as you stop the antibiotics, the Borrelia bounce back. Her lab is testing different bee venoms on all forms of the bacteria, and so far, the melittin venom seems effective...And they still don’t really know why the venom works for Ellie, not least because the exact cause of post-treatment Lyme disease symptoms remains unknown. “Is it effective for her because it’s killing Borrelia, or is it effective because it stimulates the immune system?” asks Sapi. It’s still a mystery.

Honeybee landing on milkthistle02.jpg Honeybee (Apis mellifera) - from Wikipedia 

Very interesting research that may change how we view Lyme Disease - that the bacterium Borrelia burgdorferi — the cause of Lyme disease — may be a contagious illness, sexually transmitted between partners. From the January 27, 2014 Medical Daily:

Is Lyme Disease Contagious? Clues Hint That It May Be A Sexually Transmitted Disease

 A new study published in the Journal of Investigative Medicine suggests the bacterium Borrelia burgdorferi — the cause of Lyme disease — may be a contagious illness, sexually transmitted between partners.

The transmission from person-to-person has been an idea refuted by the CDC who believes it is solely transmitted to humans through the bite of an infected blacklegged tick. “The CDC position on sexual intra-human Borrelia burgdorferi transmission is that it does not occur,” the agency said in a 2011 statement.

The study — presented at the annual Western Regional Meeting of the American Federation for Medical Research — a collaborative effort by an international team of scientists — tested semen samples and vaginal secretions of three groups of patients to investigate whether passing Lyme disease to a partner through unprotected sex is a possibility. The study observed control subjects without evidence of Lyme disease, random subjects who tested positive for Lyme disease, and married heterosexual couples engaging in unprotected sex who tested positive for the disease. The presence of B. burgdorferi and identical strains of the bacterium were of particular interest to the researchers in unprotected sex in spouses.

The control subjects were found to test negative for the bacterium in semen samples or vaginal secretions, as expected by the researchers. The researchers found traces of B. burgdorferi in the vaginal secretions of all women with Lyme disease. In contrast, approximately half of the men with the disease tested positive for the bacterium in semen samples. In addition, one of the heterosexual couples with Lyme disease were found to have identical strains of the bacterium in their genital secretions.

A surprising finding for the researchers was why women with Lyme disease had consistently positive vaginal secretions, compared with the semen samples that showed greater variability. Although this warrants further research, overall, the results indicate the presence of the bacterium in genital secretions and identical strains in married couples, which means the disease may be contracted through sexual transmission. “Our findings will change the way Lyme disease is viewed by doctors and patients,” said Marianne Middelveen, lead author of the study presented in Carmel, 

The possibility of Lyme disease being a sexually transmitted disease could help explain the increase in reported cases throughout the years, suggesting ticks aren’t the only way of infection. The disease is commonly undiagnosed due to the signature “bull’s eye rash” absence in nearly half of those who are infected.