Archive for the ‘research’ Category

B. Miyamotoi in CA Ticks For a Long Time

The following article explains that Borrelia Miyamotoi is not new to California.  First considered nonpathogenic, it wasn’t even reported until 2011 in Russia.  Diagnosis relies on PCR testing during acute infection and two-tiered testing for Lyme will not pick it up.  It is not a reportable illness so prevalence is pure conjecture.  Dr. Horowitz states clinicians should be vigilant for clinical pictures that look like viral infections such as high fever, headache, and muscle and joint pain.  In publications, only 16% of patients presenting with BMD were seropositive for IgG and/or IgM antibody to B. miyamotoi rGlpQ, so PCR should also be considered in patients with a history of tick bites and appropriate clinical manifestations.

This is also an important reminder that new strains and species are being discovered continually, so nothing about Tick Borne Illness should be set in stone and open minds are a must. (Study found here)  by Lonnie Marcum

LYME SCI: B. miyamotoi has been in California ticks for a long time

Like forensic detectives, using a bank of frozen blood serum from the 1980s, tick researchers from both the west and east coasts set out to determine how prevalent Borrelia miyamotoi infection is in California. What they discovered should set off more than a few alarms.

B. miyamotoi is a spiral-shaped bacterium in the same genus as Borrelia burgdorferi, the agent of Lyme disease. But it is most closely related to the group of relapsing fever Borrelia spirochetes. It has recently been recognized as causing a form of borreliosis that is similar to Lyme disease—Borrelia miyamotoi disease (BMD).

B. miyamotoi is transmitted by the same hard-bodied ticks that carry Lyme disease—the blacklegged or deer tick (Ixodes scapularis) and the western blacklegged tick (Ixodes pacificus).

The symptoms of BMD are similar to Lyme disease but generally more severe, with the addition of a relapsing fever, and the absence of a typical bull’s-eye rash. Because BMD is not a reportable disease in the US, there is very little information about its symptoms or prevalence.

For this study, the researchers were given access to a biobank of 101 blood samples collected from a rural community in Mendocino County, California, after an outbreak of Lyme disease in the late 1980s. The area has since been the focus of many tick studies and is known for high prevalence of ticks that carry both BMD and Lyme disease.

Three quarters of the people in the study reported frequent tick bites in the one to two years prior to the blood draw. Later, a confirmatory blood test showed that 79% had antibodies to tick salivaa rate nearly three times that of residents of Block Island, Rhode Island (29%), where Lyme disease is highly endemic.

For the BMD screening, researchers used two different methods to look for evidence of prior exposure to B. miyamotoi—a two-step glycerophosphodiester phosphodiesterase enzyme-linked immunosorbent (rGlpQ) assay and a whole-cell lysate (WCL) assay.

Twenty-six of the 101 samples were reactive for BMD. [Note: the B. miyamotoi GlpQ assay is not affected by Lyme disease infection because B. burgdorferi does not produce GlpQ antigen.]

The samples were also tested for Borrelia hermsii and Borrelia burgdorferi, to examine the possibility of cross-reactivity and/or dual infection.

The researchers feel there is probable cause of BMD infection for several reasons:

Studies showing 0.5% to 15% of Ixodes pacificus ticks carry B. miyamotoi infection in Northern California, B. miyamotoi is passed from parent to offspring (transovarial transmission), increasing risk of infection from nymphal ticks, and mild climates allow for nearly year-round activity of ticks in California.

“No human cases of B. miyamotoi previously have been reported from the western United States even though I. pacificus ticks in northern California have a spirochete-infection prevalence similar to or exceeding that of I. scapularis ticks in the Northeast and upper Midwest,” according to the authors.

The authors go on to warn, “Healthcare professionals in the far-western United States should be aware that B. miyamotoi disease may occur throughout the geographic distribution of I. pacificus and that improved relapsing fever group spirochete antibody assays are urgently needed.”

In summary, while B. miyamotoi is considered an “emerging” infectious disease, it is not new to California. The fact that there are no previously reported cases is because 1) until recently there have been no commercially available tests and 2) since BMD is not a reportable disease, nobody collects such information.

This study highlights the pressing need to develop better diagnostic tests capable of detecting all tick-borne diseases–and to collect the results of those tests in a way that’s accessible to the public.

LymeSci is written by Lonnie Marcum, a Licensed Physical Therapist and mother of a daughter with Lyme. Follow her on Twitter: @LonnieRhea Email her at: .



Interestingly, the CDC states that PCR and antibody-based testing for Bm are under development and not widely available but can be ordered from a few CLIA-approved labs.

Now that’s sweet isn’t it?  Up until now the CDC has vilified all CLIA approved labs – especially for Lyme testing.

Dr. Cameron points out the hypocrisy marvelously here:  Researchers have had to diagnose B. miyamotoi based on blood smear, direct detection of spirochetes in cerebrospinal fluid and follow-up polymerase chain reaction (PCR) and molecular detection of B. miyamotoi DNA in acute whole blood from patients.  These are all non FDA-approved tests. So, where would these patients be if the FDA insisted on only its tests being utilized?

You gotta love fate.





Bb in Small Kentucky Mammals

Borrelia burgdorferi in small mammal reservoirs in Kentucky, a traditionally non-endemic state for Lyme disease

Buchholz MJ, Davis C, Rowland NS, Dick CW.
Parasitology Research, online first 2018 Feb 7.


The incidence of tick-borne zoonoses such as Lyme disease has steadily increased in the southeastern United States. Southeastern states accounted for 1500 of over 28,000 confirmed cases of Lyme disease reported in the United States during 2015. Borrelia burgdorferi, the etiologic agent of Lyme disease, is maintained in small mammal reservoirs and vectored to new hosts by ixodid ticks.

This study examined ecological relationships of the B. burgdorferi/vector/reservoir system in order to understand the dynamics of Lyme disease risk in Kentucky. Small mammals were captured using live traps from November 2014 to October 2015. Ticks were removed and blood and tissue collected from small mammals were screened for B. burgdorferi DNA by PCR with primers specific to the OspA gene.

Prevalence of B. burgdorferi (21.8%) in Kentucky small mammals was comparable to the lowest recorded prevalence in regions where Lyme disease is endemic. Moreover, infestation of small mammals by Ixodes scapularis, the primary vector of B. burgdorferi, was rare, while Dermacentor variabilis comprised the majority of ticks collected.

These findings provide ecological insight into the relative paucity of Lyme disease in Kentucky.



The conclusion of this study is all wrong.  Bb was found Kentucky mammals.  That in itself is important.  Also, the fact the preponderance of ticks were dermacentor variabilis (wood tick or American dog tick) which supposedly has not been proven to be a competent vector of Bb as supposedly it doesn’t efficiently pass Bb from inside the tick to humans or other hosts), it does transmit Tularemia and Rocky Mountain Spotted Fever.

BTW:  these transmission studies given as references for this fact were done from 1997-2006.  It’s now 2018.  Notice it states, “It doesn’t efficiently pass Bb.”  What if it passes it inefficiently?  It still passes!

Regardless of whether the wood tick can transmit Bb or not, they do transmit pathogens.  The fact that nearly 22% of small Kentucky mammals have Bb due to the black legged deer tick and most of the ticks they picked up were wood ticks, those deer ticks were particularly infected.

Hear ye, hear ye, the South has Lyme.

For more:  According to Dr. Naveen Patil, Director of the Infectious Disease Program, ADH,

We don’t have Lyme Disease in Arkansas, we have the ticks that transmit Lyme Disease but we don’t have any recorded cases of Lyme Disease.”  A news report emphasizing the CDC’s belief Arkansas is a “low incident” state in regards to Lyme Disease, is countered by the Arkansas Lyme Foundation that claims at least 150 cases, and they just started counting. (Video here)

People are dying and I’m not exaggerating, people are calling us every week in desperate situations,” said Sikes.  Last summer, a friend who lives in Oklahoma found a classic bullseye rash on her seven-year-old daughter.

“That’s a spider bite,” a local pediatrician told her. “We don’t have Lyme in Oklahoma.”

The doctor was wrong. Had my friend taken his advice, her daughter would not have been diagnosed in a timely fashion and she would likely have developed symptoms over the next few months or years. She probably would have become severely debilitated, and the infections might have crossed the blood-brain barrier and become chronic.

Get the picture yet?  Lyme/MSIDS is everywhere.

Quit saying it’s rare!

Borrelia Miyamotoi in CA: Serodiagnosis is Complicated by Multiple Endemic Borrelia Species

Human Borrelia miyamotoi infection in California: Serodiagnosis is complicated by multiple endemic Borrelia species

Krause PJ, Carroll M, Fedorova N, Brancato J, Dumouchel C, Akosa F, Narasimhan S, Fikrig E, Lane RS.
PLoS One. 2018 Feb 8;13(2):e0191725. eCollection 2018.


To determine whether human Borrelia miyamotoi infection occurs in the far-western United States, we tested archived sera from northwestern California residents for antibodies to this emerging relapsing fever spirochete. These residents frequently were exposed to I. pacificus ticks in a region where B. miyamotoi tick infection has been reported.

We used a two-step B. miyamotoi rGlpQ assay and a B. miyamotoi whole-cell lysate (WCL) assay to detect B. miyamotoi antibody. We also employed Borrelia hermsii and Borrelia burgdorferi WCL assays to examine if these Borrelia induce cross reacting antibody to B. miyamotoi. Sera were collected from 101 residents in each of two consecutive years.

The sera of 12 and 14 residents in years one and two, respectively, were B. miyamotoirGlpQ seroreactive. Sufficient sera were available to test 15 of the 26 seropositive samples using B. miyamotoi and B. hermsii WCL assays. Two residents in year one and seven residents in year two were seroreactive to both Borrelia antigens.

Although discernible differences in seroreactivity were evident between the B. miyamotoi and B. hermsii WCL assays, infection with one or the other could not be determined with certainty. Sera from two Borrelia burgdorferi /B. miyamotoi seropositive subjects reacted strongly against B. miyamotoi and B. hermsii WCL antigens. Ecological, epidemiological, and clinical data implicated B. miyamotoi as the probable cause of infection among those whose sera reacted against both antigens.

Our findings suggest that human B. miyamotoi infection occurs in northern California and that B. hermsii and B. burgdorferi infections produce antibodies that cross-react with B. miyamotoi antigens. Health care professionals in the far-western United States should be aware that B. miyamotoi disease may occur throughout the geographic distribution of I.pacificus and that improved relapsing fever group spirochete antibody assays are urgently needed.




This study points out one the biggest reasons we are in this quagmire:  poor testing and cross reactivity of antigens.  Remember, testing for miyamotoi is new so folks could have been infected with this pathogen for a long time and it flew under the radar. They got tested for borrelia burgdorferi (Lyme) with a test that misses over half of all cases, and are sent home and told, “Go home and be well.”  

There very probably are other strains and pathogens we don’t have testing for yet.

It also demonstrates Tick borne illness is everywhere, despite Speilman’s maps:  (Scroll down to comment section after article)




Study Shows Mycobacterium Infected Animal Products Linked to Rheumatoid Arthritis in the Genetically Predisposed

Study Finds Bacteria in Milk Linked to Rheumatoid Arthritis

Study Finds Bacteria in Milk Linked to Rheumatoid Arthritis

A strain of bacteria commonly found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are genetically at risk, according to a new study from the University of Central Florida.

A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.

The UCF researchers are the first to report this connection between MAP and rheumatoid arthritis in a study published in the Frontiers in Cellular and Infection Microbiology journal this week. The study, funded in part by a $500,000 grant from the Florida Legislative, was a collaboration between Saleh Naser, UCF infectious disease specialist, Dr. Shazia Bég, rheumatologist at UCF’s physician practice, and Robert Sharp, a biomedical sciences doctoral candidate at the medical school.

Naser had previously discovered a connection between MAP and Crohn’s disease and is involved in the first ever phase III-FDA approved clinical trial to treat Crohn’s patients with antibiotics. Crohn’s and rheumatoid arthritis share the same genetic predispositions and both are often treated using the same types of immunosuppressive drugs.  Those similarities led the team to investigate whether MAP could also be linked to rheumatoid arthritis.

“Here you have two inflammatory diseases, one affects the intestine and the other affects the joints, and both share the same genetic defect and treated with the same drugs. Do they have a common trigger? That was the question we raised and set out to investigate,” Naser said.

For the study, Bég recruited 100 of her patients who volunteered clinical samples for testing.  Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn’s patients, and 40 percent of that number tested positive for MAP.

“We believe that individuals born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis,” Naser said.

About 1.3 million adults in the U.S. have rheumatoid arthritis – an autoimmune and inflammatory disease that causes the immune system to attack a person’s joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women.

Although case studies have reported that some RA patients suffer from Crohn’s disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.

“We don’t know the cause of rheumatoid arthritis, so we’re excited that we have found this association,” Bég said. “But there is still a long way to go.  We need to find out why MAP is more predominant in these patientswhether it’s present because they have RA, or whether it caused RA in these patients. If we find that out, then we can target treatment toward the MAP bacteria.”

The team is conducting further studies to confirm findings and plan to study patients from different geographical and ethnic backgrounds.

“Understanding the role of MAP in rheumatoid arthritis means the disease could be treated more effectively,” Naser said.  “Ultimately, we may be able to administer a combined treatment to target both inflammation and bacterial infection.”

Naser holds a Ph.D in Medical Microbiology from New Mexico State University. He joined UCF in 1995. He has been investigating Crohn’s disease and other auto-immune diseases for more than 30 years. He has published more than 100 peer-reviewed articles and has presented his work at numerous conferences.  He has several patents including a licensed DNA technology for detecting MAP.

Bég, a board-certified rheumatologist, has been with UCF since 2011 after completing her fellowship in rheumatology at Baylor College of Medicine in Houston. In addition to practicing medicine at UCF Health, she is a full-time faculty member at the college. Her research and clinical interests include conditions such as rheumatoid arthritis, psoriatic arthritis, lupus and osteoporosis.



Lyme/MSIDS patients need to take note of this study as RA is often undiagnosed tick-borne infections – including Mycoplasma.  The genetic issue as well as consuming infected animal products should be a concern to us all; however, being infected with TBI’s is right up there on the list.

BTW:  Garth Nicholson has been sleuthing on the role of Mycoplasma and Lyme/MSIDS for years:

And previously to that, Dr. Brown way back in the 40’s and 50’s believed that RA was caused by mycoplasmas and used tetracycline rather than prednisone, the drug of choice. He eventually modified his treatment which included Minocycline and brought over 10,000 patients into remission.  (This demonstrates the importance of dealing with the infection)

I find it interesting that Minocycline was probably the drug that helped me the most:  This link also shows Nicholson’s discovery that 90% of evaluated ALS patients had Mycoplasma. 100% of ALS patients with Gulf War Syndrome had Mycoplasma and nearly all of those were specifically the weaponized M. fermentans incognitos.  One of the hallmark symptoms of Mycoplasma is fatigue.
And the bad news for us is that Nicholson’s experience has found Mycoplasma to be the number one Lyme coinfection, and similar to other coinfections in that it can be supposedly cleared for years only to reappear when conditions are right.

One other note is that immunosuppressive drugs for folks that have TBI’s are going to worsen their condition, so TBI’s must be ruled out before the administration of them, which is going to be tricky business as the tests for all of these pathogens is abysmal.  I highly recommend having patients fill out the Horowitz questionnaire along with testing and for doctors to make a clinical diagnosis not based on testing only:

This study also shows the dire need for medical professionals to be properly trained regarding TBI’s or they run the risk of putting patients on immunosuppressive drugs to their demise.  So far the education in med school on Tick borne infections is antiquated and brief, considering Lyme is the #1 vector borne disease in the U.S.  No one has accurate numbers on coinfections.  If you know of doctors who are willing to be trained in this area, please send them this: Betty Maloney, President, Partnership for Tick-borne Diseases Education created a website built specifically for the purpose of offering accredited, evidence-based continuing medical education (CME) modules on Lyme and other tick-borne diseases (TBD) for doctors and other healthcare professionals. Doctors will like the convenience of on-demand learning that’s available on PC and mobile devices. The modules I developed for LymeCME provide a concise review of the evidence, highlighting points that are especially relevant to patient care. And, they’re free!

More on Myco:  Dr. Rawls states:  “Borrelia, the microbe commonly associated with Lyme disease, could be a culprit. However, I would lay odds on mycoplasma and a closely related bacterium called ureaplasma. About 75% of chronic Lyme disease sufferers have been found to harbor at least one species of mycoplasma.

It fits. Mycoplasma and ureaplasma are the smallest of all bacteria. They are obligate intracellular microbes — which means they must live inside cells of a host to survive. They typically infect linings of the body — linings of lungs, intestines, joints, and the urinary tract.
Different species of mycoplasma and ureaplasma prefer certain areas of the body, but any species of these microbes can be found in different places the body. The most common species found in the urinary and reproductive tract are Ureaplasma urealyticum and Mycoplasma hominis. These microbes typically spread sexually, but they can be acquired by other routes. Mycoplasma pneumoniae, a frequent cause of respiratory infections, can also be found in the urinary tract.  Mycoplasma and ureaplasma are notoriously difficult to culture.”

But back to Mycobacterium…..Dr. Horowitz is finding that Mycobacterium drugs are working for his treatment resistant patients:    The case study has based on a woman with Borrelia burgdorferi, Borrelia hermsii, possible prior exposure to tularemia, exposure to Mycoplasma pneumonia, multiple viruses, fibromyalgia, and rheumatoid arthritis.
Under Dr. Horowitz’s care she improved from 30% to 50%, but with the addition of Dapsone had a sudden fourfold increase in tularemia titers as well as Bartonella titers turning positive.  While making continuous progress the patient had ongoing joint pain which interfered with sleep as well as ongoing severe blood-filled blisters, oral/genital ulcerations, and increased granulomas.
While a rheumatologist wanted to put her on an immunosuppressive, she and Dr. Horowitz chose to try 500mg (based on body weight) of PZA twice a day combined with rifampin and minocycline. Her liver was monitored every two weeks and was helped with alpha lipoid acid 600mg and milk thistle 250mg.  Two months later she reported up to 80% of normal functioning…

The fact that the addition of a mycobacterium drug that gave this woman 80% of normal functioning is something that needs to be noted.  It also leads to the conclusion that her prior diagnosis of RA is probably infectious in nature and improved with microbials.

Now if that isn’t a success story, I don’t know what is.  So something is going on here with Mycobacterium or a mycobacterium-like pathogen.  This needs to be hunted to ground.



Lyme in the Southern Hemisphere & Sexual Transmission  By Dr. Jose’ Lapenta

Hello friends of the network, DERMAGIC EXPRESS brings you today another interesting topic, which perhaps you had never imagined: THE LYME DISEASE SEXUAL TRANSMISSION AND ARRIVAL IN THE SOUTHERN HEMISPHERE, Disease that since its discovery and description was first attributed to the locality of LYME in Connecticut, US, and today described worldwide in NORTH HEMISPHERE, EUROPE, ASIA, (EURASIA) and the AFRICAN continent. It also raises the possibility that it is a Sexually Transmitted disease

With numerous cases on the rise each year, disease caused by the already mentioned in previous reviews THE BORRELIA BURGORFERI, A ESQPIROCHETE, which is very difficult to treat because of the resistance it offers to the treatment and because of its “ability” to “hide before the tests from laboratory.

As I said in the previous review, THE TICKS are a “BIBLE PEST”, mentioned in the book of the BIBLE, BOOK EXODUS:

“… And the dust of the earth became lice throughout the land of Egypt” … a well-knowledgeable tourist from Egypt observed that the sand seemed to move; observing more closely, he saw that the surface of the earth was a mass of tiny ticks … ”

So here comes the following observation: if it is a “BIBLE PLAGUE” such as LEPROSY AND SYPHILIS, it should be disseminated throughout the world, not just to a certain region, right?

Well, here I am going to show you that the BORRELIA BURGDORFERI, several years ago was described in several countries of South America, making this disease (LYME or ERYTHEMA MIGRANS) a global pathology; and I will mention one by one the countries where it was described with their respective observations:

The complex BORRELIA BURGDROFERI sensu lato (sl) includes agents of Lyme disease / borreliosis in NORTH AMERICA, EUROPE AND ASIA. Such as BORRELIA BURGDORFERI sensu stricto (st), Borrelia afzelii, Borrelia garinii, Borrelia bavariensis, Borrelia spielmanii, Borrelia bissettiae and Borrelia mayonii. In short: BORRELIA sensu stricto(st): LYME DISEASE in North America, South America? BORRELIA sensu lato (sl): LYME DISEASE in EUROPE AND ASIA, SOUTH AMERICA.

In the year 2013, a study was made looking for BORRELIA sensu lato (sl) ESPIROCHETES related to species of TICKS belonging to the complex IXODES RICINUS which classically inhabit the NORTHERN HEMISPHERE, in this study the BORRELIAL infection was studied in the TICK IXODES PARARICINUS, unique species that represents the IXODES RICINUS complex in URUGUAY. Were studied 137 ticks obtained from DEER, CATTLE or VEGETATION, in 2 Uruguayan departments. It was detected by means of laboratory studies, PCR, haplotype studies, infection in 9 MALES and a group of nymphs sequences for BORRELIA BISSETTII, a species very close to American borrelia. The authors considered their study the first report of infectious ticks of BORRELIA BURGDORFERI sensu lato (sl) in South America.

Prior to this study in 2005, another investigation was made where a collection of the IXODES PARARICINUS TICKS were made, in URUGUAY and ARGENTINA, which was first described by Keirans and Cliford in 1.985, of fatted females collected from CATTLE and larvae fed with MICE AND CHICKENS. A taxonomic study was made of IXODES PARARICINUS, which is geographically distributed in: URUGUAY, ARGENTINA, and COLOMBIA, but is probably established in other countries such as BOLIVIA, BRAZIL, CHILE and PERU. It has also been found in RODENTS AND WILD BIRDS. It stands out in the study that thisTICKS is part of the IXODES PARARICINUS complex, vector of BORRELIA BURGDORFERI sensu lato (sl).

Also in Uruguay IXODES PARARICINUS was collected in the birds Turdus albicollis, Turdus rufiventris Vieillot, Syndactyla rufosuperciliata, and Basileuterus leucoblepharus, these birds have their habitat in the forests of: URUGUAY, ARGENTINA CHILE, PARAGUAY, BRAZIL, BOLIVIA, AND PERU.

In the year 2104, the criterion was unified that the IXODES PARARICINUS tick was previously described in the year 1998. Under the name of IXODES ARAGOI FONSECA, a controversy remained for years, until the last studies concluded that phylogenetically the difference between the two is minimal, being then its ORIGINAL name IXODES ARAGOI, with the pseudonym IXODES PARARICINUS.

CONCLUSION: BORRELIA BURGDOERFERI sensu lato (sl) is circulating at SOUTHERN HEMISPHERE, in URUGUAY, COLOMBIA, BOLIVIA, PARAGUAY and other countries that I describe below:

The case of BRAZIL is quite interesting, in the year 1992 a disease was described in HUMANS, in two siblings WITH ALL THE CHARACTERISTICS OF THE LYME DISEASE, after being bitten by ticks. The researchers were Domingos Baggio, entomologist and doctor Natalino Hajime Yoshinari. The disease under study was not recognized as A CLASSIC LYME, because the ticks did not belong to the IXODES RICINUS complex and the laboratory was negative for BORRELIA BURGDORFERI, but under an electron microscope it was detected that the causative organism was from the PHYLUM “ESPIROCHETE”.

It was classified as a new emerging zoonosis in BRAZIL under the name of BAGGIO YOSHINARI SYNDROME (BYS), practically a variant of LYME disease in the American continent, caused by the sting of TICKS, with the same clinical characteristics with the exception of with autoimmunity and recurrence.

In 2013, BORRELIA BURDORGFERI was reported in the tropical Neo region in the PAMPA URUGUAYA, isolated from the TICK IXODES ARAGOI, and between 2011 and 2016, 17 suspected cases of BORRELIOSIS SYNDROME were reported in the South of Brazil, DNA positive for BORRELIA. spp in ticks of the genus IXODES spp, specifically IXODES LONGISCUTATUS, the deepest study of haplotypes approached the species to: Borrelia carolinensis, B. bissettiae and Borrelia californiensis. Becoming the first evidence of the circulation of BORRELIA BURGDORFERI sensu lato in ticks of the genus IXODES spp IN BRAZIL, in other words the causal agent of the LYME DISEASE.

In the year 2014, a study was conducted in the rural area of ​​the state of Paraná, in BRAZIL, and the presence of BORRELIA GARINII and BORRELIA BURGDORFERI sensu stricto (st) was detected through PCR studies and DNA sequencing in Brazilian individuals, suggesting circulations these species in BRAZIL.

In that same year 2014 another study was made in that same area of ​​Paraná Brazil, collecting 224 TICKS on traction horses, (75%) of the gender DERMACENTOR NITENS and 25% AMBLYOMMA CAJANENSE, in two cases (Dermacentor nitens ticks) positivity was found for BORRELIA BURGDORFERI sensu lato, but the most interesting thing is that the DNA sequence by PCR revealed a 99.99% homology with the BORRELIA BURGDORFERI Sensu sricto (st) strain B31, another one of the strains causal agent of LYME DISEASE IN USA

In January of this year 2018 a study was carried out in BRAZIL also in horses: The objective of this study was to detect and measure the frequency of anti-BORRELIA IgG antibodies. burgdorferi American strain G39 / 40 on horses in the municipality of Sinop, MT-Brazil in the state of Mato Grosso, SEEKING EVIDENCE of the presence of the BORRELIA sensu stricto (st) which is the main causative agent of LYME DISEASE in the United States , because it is believed that a SIMILAR ESPIROQUETA is the causal agent of the BAGGIO YOSHINARI SYNDROME that I mentioned at the beginning, and of 367 horses studied 214 were POSITIVE for BORRELIA sensu stricto (78%) and in at least 75 farms there was a positive horse for BORRELIA BRURGDORFERI (92.59%) of the total, a high animal prevalence.

CONCLUSION: BORRELIA BURGORGFERI sensu stricto and sensu lato are circulating in the SOUTHERN HEMISPHERE IN BRAZIL and the BAGGIO YOSHINARI SYNDROME which has been considered a variant of the classic LYME DISEASE in this continent MAYBE IT IS THE SAME LYME DISEASE or ERYTHEMA MIGRANS as such.

3.) CHILE:
In the year 2014, a study was made in CHILE, where BORRELIA BURGDORFERI sensu lato (sl) was reported in endemic IXODES STILESI ticks collected in Chile from environmental vegetation and long-tailed rice rats (Oligoryzomys longicaudatus). The phylogenetic analysis placed this spirochete as a new genospecies within the Lyme borreliosis group; and the appointment of this new South American member of the LYME BORRELIA CHILENSIS VA1 borreliosis group was proposed in honor of the country of origin.

In another more recent study in 2017, it was determined that this IXODES STILESI tick also infects mice, in the South of Chile, the Pudú deer (pudu Puda). Sixty-six deer were examined over a period of two years. A total of 179 ticks of two species, IXODES STILESI and IXODES TAGLEII were collected, and BORRELIA ESPIROCHETES were found in 2 (6.45%) of the ixodes stilensi ticks, being this genetically the same as the BORRELIA CHILENSIS VA1 previously described in Chile, that which can play an important role in the prevalence of BORRELIA in that country and more studies are suggested to understand a possible pathogenicity towards humans.

CONCLUSION: BORRELIA CHILENSI V1A sensu lato (sl) is circulating in CHILE, through the IXODES STILENSI tick, hosts: the mouse Oligoryzomys longicaudatus and the Pudú Puda deer. The habitat of these 2 animals also includes ARGENTINA.

Turdus rufiventrus (rufous-bellied thrush), (Syndactyla rufosuperciliata (buff-browed foliage-gleaner), Basileuterus leucoblepharus ( white-rimmed warbler) and seabird, 4 birds that are carriers of the tick IXODES PARARICINUS, and lives in the forest and sea of : URUGUAY, ARGENTINA CHILE, PARAGUAY, BRAZIL, BOLIVIA, AND PERU.

In the year 2014, a study was made on IXODES PARARICINUS ticks collected from the vegetation of the Province of Jujuy in ARGENTINA, to determine infection by BORRELIA through PCR. A male and a female of I. pararicinus collected in Jujuy were positive for Borrelia infection. Phylogenetically, THE BORRELIA found in I. pararicinus of Jujuy belongs to the complex B. BURGDORFERI sensu lato (sl), and was similar to one of the genospecies detected in IXODES ARAGOI of Uruguay. In addition, this genospecies is closely related to two known genospecies of EE. UU., Borrelia americana and Borrelia sp. Genospecies 1.

In the year 2017, another study was carried out in ARGENTINA, collecting TICKS and NYMPHS from IXODES PARARICINUS, vegetation and birds, in the Provinces of Jujuy, Tucumán and Salta; In total 82 ticks and several nymphs were studied both from the vegetation of Salta and the birds Turdus rufiventris in Tucumán, Syndactyla rufosuperciliata in Jujuy and Turdus nigriceps in Tucumán. Two (2) haplotypes of BORRELIA sp. Belonging to the BORRELIA BURGDORFERI sensu lato complex. One of them is closely related to the Borrelia genoespecies haplotypes previously reported in IXODES ARAGOI of Uruguay and IXODES. PARARICINUS from the province of Jujuy in Argentina. The authors mention that these IXODES species do not represent pathogenicity for humans. However, others say that further studies are needed to verify this claim.

More recently this year 2018 was conducted another study to investigate the presence of TICKS THAT INFECT cattle in the province of Yungaos in ARGENTINA with BORRELIA, ERLICHIOSIS and RICKETTSIA, the study showed once again that ticks of the genus IXODES PARARICINUS positive were found for BORRELIA BURGODRFERI sensu lato (sl), as I said previously phylogenetically related to IXODES ARAGOI of URUGUAY.


In 1999, the presence of specific IgG antibodies for BORRELIA BURGDORFERI in patients with clinical manifestations of LYME DISEASE was evaluated in COLOMBIA. Were analyzed 20 samples of symptomatic patients, 1 sample of cerebrospinal fluid (CSF) of a patient with chronic and arthritic neurological manifestations and 12 samples of patients with suspicion of Lyme BORRELIOSIS, being positive in 4 samples of symptomatic patients, 2 with morphea they were positive as well as the patient with neurological manifestations. The work proposes to analyze with “caution” this disease “type lyme” and suggest that a genoespecies BORRELIA different from the sensu stricto (st) is the causal agent, In other words BORRELIA sensu lato (sl) another LYME DISEASE CAUSAL AGENT.

CONCLUSION: BORRELIA BURGDORFERI sensu lato (sl) is probably the causal agent of LYME “type” DISEASE in COLOMBIA.

6.) PERU:
In the year 1999, a study was made in the Andean areas of Peru in search of bacterial infections associated with lice, prevalence of EPIDEMIC OF TIFFUS, TRENCH FEVER AND RECURRENT FEVER. Were included 194 volunteer inhabitants of the province of Calca in the Urbamba valley. Thirty-nine (20%) of the 194 volunteers had antibodies against Rickettsia prowazekii, while 24 (12%) had antibodies against Bartonella quintana and 2 against BORRELIA recurrentis.

CONCLUSION: There are no studies that confirm the PRESENCE OF BORRELIA BURGDORFERI in Peru, but the PRESENCE OF BORRELIA RECURRENTIS causal agent of the RECURRENT FEVER, was found, whose causal agent is also a BORRELIA, ESPIROCHETE, and transmitted by the bite of lice; but remember that there are 4 species of birds that carry the TICK IXODES PARARICINUS (Borrelia sensu lato sl) that circulate in the forests of PERU.

And the plague came to VENEZUELA also, between the year 1992 and 1993, 74 patients were studied in Zulia State: 37 asymptomatic and 37 clinically suspects of LYME DISEASE, ELISA tests were performed and positive cases were found for BORRELIA BURGDORFERI sp: 14 of 74 (18.9%). Positive cases in the symptomatic group (29.7%) were higher than in the asymptomatic group (8.9%). The most frequent clinical diagnosis was Morphea (54.5%). The main serological diagnosis (54.32%) was obtained from chronic patients (more than one year of evolution). 45.5% of the symptomatic patients presented antibodies, despite receiving antibiotic treatment. Most of the cases had a previous visit or stay in forest or rural areas.

The authors affirm the presence of BORRELIA BURGDOFERI and LYME DISEASE in patients from the State of Zulia VENEZUELA and propose more precise studies such as the immunoblot. The relationship between MORPHEA and infection with BORRELIA is well known in the international DERMATOLOGICAL community.


And what do you think if I tell you that there are VARIOUS studies confirming a “probable transmission of LYME DISEASE through sexual intercourse”, vaginal and seminal fluid, I must remind you that BORRELIA is a SPIROCHETE same as SYPHILIS, and the latter is transmitted by seminal and vaginal fluid; why the BORRELIA NOT?

The first study dates from the year 2001, that is 17 years ago, which was presented at an international conference on LYME disease, in which 40% of positivity was demonstrated by PCR in semen samples (14 of 32 patients). and 1 case of vaginal fluid.

“… ALL positive semen / vaginal samples in patients with known sexual partners resulted in positive Lyme / PCR titers in their sexual partners, 3/4 patients with positive semen had unknown or unknown sexual partners to be evaluated. .. “

Another study dates from the year 2014, January 25, the researchers tested samples of semen and vaginal secretions from three groups of patients: control subjects without evidence of Lyme disease, random subjects who tested positive for Lyme disease and married heterosexual couples who had sex unprotected and tested positive for the disease.

As expected, all control subjects were negative for BORRELIA BURGDORFERI in semen samples or vaginal secretions. In contrast, all women with Lyme disease tested positive for BORRELIA BURGDORFERI in vaginal secretions, while approximately half of men with Lyme disease tested positive for Lyme spirochete in semen samples. In addition, one of the heterosexual couples with Lyme disease showed IDENTICAL STRAINS of the Lyme spirochete in their genital secretions.

“There is always some risk of getting Lyme disease from a bite in the forest,” he said. “But there may be an increased risk of getting Lyme disease in the bedroom.”

The other study dates from the year 2015 To investigate this possibility, Middelveen et al. performed the first culture study of BORRELIA in human semen and vaginal secretions.

¨ … Patients with documented LYME DISEASE, including heterosexual couples who have unprotected sex, studied genital cultures in three independent laboratories. Sperm cultures and vaginal secretions were subjected to light and dark field microscopy and were found to contain LIVING MOBILE SPIROCHETES that exhibited a characteristic wave motion and stained positively with silver Dieterlee immunostaining for B. burgdorferi.

In addition, the PCR test and molecular hybridization with highly specific DNA probes showed that living genital spirochetes were strains of BORRELIA and not treponemes. Of particular interest, it was found that a couple had BORRELIA HERMSII and not BORRELIA BURGDORFERI in their genital secretions, further implicating sexual transmission in these cases. Control subjects who tested negative for Lyme disease had no evidence of Borrelia spirochetes in their secretions … “

More studies are probably needed to confirm what these researchers have already claimed: LYME DISEASE can be transmitted sexually. We hope that the science advances without OBSTACLES towards the definitive clarification of this aspect. But the studies I show you show that it is an indisputable reality.

Would this fact help explain why this plague has spread throughout the world? sex between couples with LYME? draw your conclusions.

1.) THE LYME DISEASE no longer belongs exclusively to the NORTHERN HEMISPHERE, here are the proof that are present in the SOUTHERN HEMISPHERE. Over there I read a comment that DENGUE, ZIKA, EBOLA AND CHIKUNGUNYA WERE NOT THE NEW PEST, the new pest or plague are THE TICKS, I said this for the first time last year and I still affirm it.

2.) I invite the medical authorities of ALL the countries of the HEMISPHERE SUR, to acquire the most specific tests to diagnose the LYME DISEASE. Because it could be that you or a family member or child, has a diagnosis of JUVENILE ARTHRITIS, PAIN ON A KNEE, OR NEUROLOGICAL MANIFESTATIONS, MORPHEA, OTHERS and you may have thousands of ESPIROCHETES, BORRELIOSIS in your blood that is killing you without realizing it.

3.) And I can bet you that many doctors worldwide DO NOT EVEN KNOW what I’m talking about, because they were sold the idea that LYME’S DISEASE is only from Connecticut USA, and not a health problem that extended to all the globe; as I once said: THE NEW LEPROSY OF THE 21ST CENTURY.

4.) If it were a reality, the sexual transmission of LYME DISEASE would change the whole panorama with respect to it and maybe the “LYME WAR” that exists between ILADS International Society of Lyme Diseases and IDSA, Society of Infectious Diseases of America ARRIVES AT ITS END because the disease would be seen in another context, beyond the simple sting of a TICK in a forest, you can also acquire it in a bedroom having sex, patients would have greater access to treatment and all policies would change, that simple, end of story.

“… And God said to Moses: tell Pharaoh and his entourage, that I AM the only creator and giver of life, I will send you 10 plagues to understand … Pharaoh ignored … The plagues came , among them TICKS …. and finished with all those who did not believe him … everyone who has ulcers and their contaminated fluids will be unclean … until he heals ….. ”


They were included here in addition to SYPHILIS, GONORRHEA AND LEPROSY LYME’S DISEASE?

Greetings to all

Dr. José Lapenta.

1.) Borrelia burgdorferi sensu lato in Ixodes longiscutatus ticks from Brazilian Pampa. Ticks Tick Borne Dis. 2017 Oct;8(6):928-932. doi: 10.1016/j.ttbdis.2017.08.003. Epub 2017 Aug 23. [PUBMED] Dall’Agnol B1, Michel T2, Weck B2, Souza UA2, Webster A2, Leal BF1, Klafke GM2, Martins JR2, Ott R3, Venzal JM4, Ferreira CAS5, Reck J6.

2.) Evidence of Borrelia in wild and domestic mammals from the state of Minas Gerais, Brazil. Rev Bras Parasitol Vet. 2014 Apr-Jun;23(2):287-90. [PUBMED] Montandon CE1, Yoshinari NH2, Milagres BS1, Mazioli R1, Gomes GG1, Moreira HN1, Padilha Ade F3, Wanderley GG4, Mantovani E2, Galvão MA3, Langoni H4, Mafra C1.

3.) The Confounding Debate Over Lyme Disease in the South The debilitating tick-borne disease is well-documented north of the Mason-Dixon line, but does it exist beyond that?
By Wendy Orent|Wednesday, December 11, 2013.

4.) Borrelia burgdorferi sensu lato in humans in a rural area of Paraná State, Brazil. Braz J Microbiol. 2015 Jun 1;46(2):571-5. doi: 10.1590/S1517-838246220140097. eCollection 2015 Jun. [PUBMED] Gonçalves DD1, Moura RA2, Nunes M3, Carreira T3, Vidotto O4, Freitas JC4, Vieira ML3.

5.) Ticks on passerines from the Archipelago of the Azores as hosts of borreliae and rickettsiae. Ticks Tick Borne Dis. 2015 Jul;6(5):607-10. doi: 10.1016/j.ttbdis.2015.05.003. Epub 2015 May 11.[PUBMED] Literak I1, Norte AC2, Núncio MS3, de Carvalho IL4, Ogrzewalska M5, Nováková M6, Martins TF7, Sychra O8, Resendes R9, Rodrígues P10.

6.) First record of Borrelia burgdorferi B31 strain in Dermacentor nitens ticks in the northern region of Parana (Brazil). Braz J Microbiol. 2014 Jan 15;44(3):883-7. eCollection 2013. [PUBMED]Gonçalves DD1, Carreira T2, Nunes M2, Benitez A1, Lopes-Mori FM1, Vidotto O3, de Freitas JC3, Vieira ML2.

7.) Regarding Tick-Borne Relapsing Fever in the Americas; Some Historical Aspects of a Forgotten Disease in Colombia. Vet Sci. 2016 Nov 4;3(4). pii: E33. doi: 10.3390/vetsci3040033. [PUBMED] Faccini-Martínez ÁA1, Botero-García CA2.

8.) Presence of Borrelia in different populations of Ixodes pararicinus from northwestern Argentina. Ticks Tick Borne Dis. 2017 Jun;8(4):488-493. doi: 10.1016/j.ttbdis.2017.02.008. Epub 2017 Feb 27. [PUBMED] Saracho Bottero MN1, Sebastian PS2, Carvalho LA3, Claps LG4, Mastropaolo M5, Mangold AJ1, Venzal JM3, Nava S6.

9.) Borrelia infection in Ixodes pararicinus ticks (Acari: Ixodidae) from northwestern Argentina. Acta Trop. 2014 Nov;139:1-4. doi: 10.1016/j.actatropica.2014.06.010. Epub 2014 Jun 28. [PUBMED]Nava S1, Barbieri AM2, Maya L3, Colina R3, Mangold AJ4, Labruna MB2, Venzal JM5.

10.) Borrelia burgdorferi sensu lato in Ixodes cf. neuquenensis and Ixodes sigelos ticks from the Patagonian region of Argentina. Acta Trop. 2016 Oct;162:218-21. doi: 10.1016/j.actatropica.2016.06.030. Epub 2016 Jun 29. [PUBMED] Sebastian PS1, Bottero MN2, Carvalho L3, Mackenstedt U4, Lareschi M5, Venzal JM3, Nava S2.

11.) Borrelia burgdorferi sensu lato infecting ticks of the Ixodes ricinus complex in Uruguay: first report for the Southern Hemisphere. Vector Borne Zoonotic Dis. 2013 Mar;13(3):147-53. doi: 10.1089/vbz.2012.1102. Epub 2013 Feb 12. [PUBMED] Barbieri AM1, Venzal JM, Marcili A, Almeida AP, González EM, Labruna MB.

12.) Ixodes (Ixodes) pararicinus Keirans & Clifford, 1985 (Acari: Ixodidae): description of the immature stages, distribution, hosts and medical/veterinary importance. Syst Parasitol. 2005 Mar;60(3):225-34. [PUBMED] Venzal JM1, Estrada-Peña A, Barros-Battesti DM, Onofrio VC, Beldoménico PM.

13.) A collection of ticks (Ixodidae) from wild birds in Uruguay. Exp Appl Acarol. 2005;36(4):325-31. [PUBMED] Venzal JM1, Félix ML, Olmos A, Mangold AJ, Guglielmone AA.

14.) Infection with Borrelia chilensis in Ixodes stilesi ticks collected from Pudu puda deer. Ticks Tick Borne Dis. 2017 Aug;8(5):733-740. doi: 10.1016/j.ttbdis.2017.05.007. Epub 2017 May 18. [PUBMED] Verdugo C1, Jiménez O2, Hernández C2, Álvarez P2, Espinoza A3, González-Acuña D4.

15.) Borrelia chilensis, a new member of the Borrelia burgdorferi sensu lato complex that extends the range of this genospecies in the Southern Hemisphere. Environ Microbiol. 2014 Apr;16(4):1069-80. doi: 10.1111/1462-2920.12310. Epub 2013 Nov 27. [PUBMED] Ivanova LB1, Tomova A, González-Acuña D, Murúa R, Moreno CX, Hernández C, Cabello J, Cabello C, Daniels TJ, Godfrey HP, Cabello FC.

16.) Genetic heterogeneity of Borrelia burgdorferi sensu lato in the southern United States based on restriction fragment length polymorphism and sequence analysis. J Clin Microbiol. 2001 Jul;39(7):2500-7. [PUBMED} Lin T1, Oliver JH Jr, Gao L, Kollars TM Jr, Clark KL.

17.) Antibody profile to Borrelia burgdorferi in veterinarians from Nuevo León, Mexico, a non-endemic area of this zoonosis. Reumatologia. 2016;54(3):97-102. doi: 10.5114/reum.2016.61208. Epub 2016 Jul 18. [PUBMED] Skinner-Taylor CM1, Flores MS1, Salinas JA2, Arevalo-Niño K1, Galán-Wong LJ1, Maldonado G1, Garza-Elizondo MA3.

18.) Genome Sequence of Borrelia chilensis VA1, a South American Member of the Lyme Borreliosis Group. Genome Announc. 2015 Feb 12;3(1). pii: e01535-14. doi: 10.1128/genomeA.01535-14. [PUBBMED] Huang W1, Ojaimi C1, Fallon JT1, Travisany D2, Maass A2, Ivanova L3, Tomova A, González-Acuña D4, Godfrey HP5, Cabello FC3.

19.) Isolation of live Borrelia burgdorferi sensu lato spirochaetes from patients with undefined disorders and symptoms not typical for Lyme borreliosis. Clin Microbiol Infect. 2016 Mar;22(3):267.e9-15. doi: 10.1016/j.cmi.2015.11.009. Epub 2015 Dec 8. [PUBMED] Rudenko N1, Golovchenko M2, Vancova M3, Clark K4, Grubhoffer L5, Oliver JH Jr6.

20.) A divergent spirochete strain isolated from a resident of the southeastern United States was identified by multilocus sequence typing as Borrelia bissettii. Parasit Vectors. 2016 Feb 4;9:68. doi: 10.1186/s13071-016-1353-4. [PUBMED] Golovchenko M1,2, Vancová M3, Clark K4, Oliver JH Jr5, Grubhoffer L6,7, Rudenko N8,9.

21.) [Detection of Borrelia burgdorferi antibodies in a population sample of the state of Zulia]. Article in Spanish] Invest Clin. 1994 Jun;35(2):91-104. [PUBMED] Arocha-Sandoval F1, Amesty-Valbuena A, Urbina M, Durango AI, Vargas-Montiel H.

22.) Survey of three bacterial louse-associated diseases among rural Andean communities in Peru: prevalence of epidemic typhus, trench fever, and relapsing fever. Clin Infect Dis. 1999 Aug;29(2):434-6. [PUBMED] Raoult D1, Birtles RJ, Montoya M, Perez E, Tissot-Dupont H, Roux V, Guerra H.

23.) Epidemiological investigation of Borrelia burgdorferi in horses in the municipality of Sinop-MT, Brazil. Trop Anim Health Prod. 2018 Jan 31. doi: 10.1007/s11250-017-1504-4. [Epub ahead of print] [PUBMED]. Socoloski SNG1, de Castro BG2, Cordeiro MD3, da Fonseca AH3, Cepeda MB3, Nicolino RR4, Lopes LB5.

24.) [Brazilian lyme-like disease or Baggio-Yoshinari syndrome: exotic and emerging Brazilian tick-borne zoonosis]. Rev Assoc Med Bras (1992). 2010 May-Jun;56(3):363-9. [PUBMED] [Article in English, Portuguese]. Yoshinari NH1, Mantovani E, Bonoldi VL, Marangoni RG, Gauditano G.

25.) Profile of patients with Baggio-Yoshinari Syndrome admitted at “Instituto de Infectologia Emilio Ribas”. Rev Inst Med Trop Sao Paulo. 2010 Nov-Dec;52(6):297-303. [PUBMED]. Gouveia EA1, Alves MF, Mantovani E, Oyafuso LK, Bonoldi VL, Yoshinari NH.

26.) Chronic lymphomonocytic meningoencephalitis, oligoarthritis and erythema nodosum: report of Baggio-Yoshinari syndrome of long and relapsing evolution. Rev Bras Reumatol. 2014 Mar-Apr;54(2):148-51. [PUBMED][Article in English, Portuguese].Rosa Neto NS1, Gauditano G2, Yoshinari NH1.

27.) Brazilian borreliosis with special emphasis on humans and horses. Braz J Microbiol. 2017 Jan – Mar;48(1):167-172. doi: 10.1016/j.bjm.2016.09.005. Epub 2016 Oct 4. [PUBMED] Basile RC1, Yoshinari NH2, Mantovani E2, Bonoldi VN2, Macoris DD3, Queiroz-Neto A3.

28.) Lyme borreliosis. An Bras Dermatol. 2010 Nov-Dec;85(6):930-8.[Article in English, Portuguese] [PUBMED] Santos M1, Haddad Júnior V, Ribeiro-Rodrigues R, Talhari S.

29. Borrelia burgdorferi infection and cutaneous Lyme disease, México. Emerg Infec Dis. 2007;13:1556-8. Emerg Infect Dis. 2007 Oct;13(10):1556-8. doi: 10.3201/eid1310.060630. [PUBMED] Gordillo-Pérez G1, Torres J, Solórzano-Santos F, de Martino S, Lipsker D, Velázquez E, Ramon G, Onofre M, Jaulhac B.

30.) Positive IgG Western blot for Borrelia burgdorferi in Colombia. Mem Inst Oswaldo Cruz. 1999 Jul-Aug;94(4):499-503. [PBMED]. Palacios R1, Osorio LE, Giraldo LE, Torres AJ, Philipp MT, Ochoa MT.

31.) Talhari S, Talhari AC, Ferreira LCL. Eritema cronicum migrans, eritema crônico migratório, doença de Lyme ou Borreliose de Lyme. An Bras Dermatol. 1992;65:205-9. [ Links ]

32.) Eritema crônico migrans/ Doença de Lyme – Estudo de três casos. XLII Congresso Brasileiro de Dermatologia, Goiânia, 1987. Talhari S, Schettini APM, Parreira VJ, Cruz RG, Melo IS, Talhari, AC.

33.) Doença de Lyme. Rio Dermatol 1988;2:4-5. Filgueira AL, Trope BM, Gontijo PP Filho.

34.) Lyme Disease May Be Sexually Transmitted, Study Suggests
source: Carmel, CA (PRWEB) January 25, 2014

35.) Sexual transmission of Lyme disease: challenging the tickborne disease paradigm. Expert Rev Anti Infect Ther. 2015;13(11):1303-6. doi: 10.1586/14787210.2015.1081056. Epub 2015 Aug 26. [PUBMED] Stricker RB1, Middelveen MJ1.

36.) Culture and identification of Borrelia spirochetes in human vaginal and seminal secretions. Version 3. F1000Res. 2014 Dec 18 [revised 2015 Apr 27];3:309. doi: 10.12688/f1000research.5778.3. eCollection 2014. [PUBMED] Middelveen MJ1, Burke J2, Sapi E3, Bandoski C3, Filush KR3, Wang Y2, Franco A2, Timmaraju A3, Schlinger HA1, Mayne PJ1, Stricker RB1.

37.) Transhemispheric exchange of Lyme disease spirochetes by seabirds. J Clin Microbiol. 1995 Dec;33(12):3270-4. [PUBMED]. Olsen B1, Duffy DC, Jaenson TG, Gylfe A, Bonnedahl J, Bergström S.

38.) BirdLife International (2012). “Basileuterus leucoblepharus”. IUCN Red List of Threatened Species. Version 2012.1. International Union for Conservation of Nature. Retrieved 16 July 2012.Taxon identifiers. Wd: Q27075948 Avibase: D65E2A9D16D052AE eBird: whbwar2 ITIS: 950065 IUCN: 22722031

39.) BirdLife International (2012). “Syndactyla rufosuperciliata”. IUCN Red List of Threatened Species. Version 2013.2. International Union for Conservation of Nature. Retrieved 26 November 2013.

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41.) Ticks infesting cattle and humans in the Yungas Biogeographic Province of Argentina, with notes on the presence of tick-borne bacteria. Exp Appl Acarol. 2018 Jan 27. doi: 10.1007/s10493-018-0208-4. [Epub ahead of print] [PUBMED] Saracho-Bottero MN1, Tarragona EL1, Sebastian PS1, Venzal JM2, Mangold AJ1, Guglielmone AA1, Nava S3.

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44.) Recovery of Lyme spirochetes by PCR in semen samples of previously diagnosed Lyme disease patients. International Scientific Conference on Lyme Disease. 2001. Available from: [Last accessed 18 April 2015] [Google Scholar] Bach G.


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Study Shows 630% More Aerosolized Flu Virus Particles Emitted by Flu-Vaccinated – A Message to Ethical MD’s

Infectious virus in exhaled breath of symptomatic seasonal influenza cases from a college community

Jing YanMichael GranthamJovan PantelicP. Jacob Bueno de MesquitaBarbara AlbertFengjie LiuSheryl EhrmanDonald K. Milton and EMIT Consortium
  1. Edited by Peter Palese, Icahn School of Medicine at Mount Sinai, New York, NY, and approved December 15, 2017 (received for review September 19, 2017)


Lack of human data on influenza virus aerosol shedding fuels debate over the importance of airborne transmission. We provide overwhelming evidence that humans generate infectious aerosols and quantitative data to improve mathematical models of transmission and public health interventions. We show that sneezing is rare and not important for—and that coughing is not required for—influenza virus aerosolization. Our findings, that upper and lower airway infection are independent and that fine-particle exhaled aerosols reflect infection in the lung, opened a pathway for a deeper understanding of the human biology of influenza infection and transmission. Our observation of an association between repeated vaccination and increased viral aerosol generation demonstrated the power of our method, but needs confirmation.


Little is known about the amount and infectiousness of influenza virus shed into exhaled breath. This contributes to uncertainty about the importance of airborne influenza transmission. We screened 355 symptomatic volunteers with acute respiratory illness and report 142 cases with confirmed influenza infection who provided 218 paired nasopharyngeal (NP) and 30-minute breath samples (coarse >5-µm and fine ≤5-µm fractions) on days 1–3 after symptom onset. We assessed viral RNA copy number for all samples and cultured NP swabs and fine aerosols. We recovered infectious virus from 52 (39%) of the fine aerosols and 150 (89%) of the NP swabs with valid cultures. The geometric mean RNA copy numbers were 3.8 × 104/30-minutes fine-, 1.2 × 104/30-minutes coarse-aerosol sample, and 8.2 × 108 per NP swab. Fine- and coarse-aerosol viral RNA were positively associated with body mass index and number of coughs and negatively associated with increasing days since symptom onset in adjusted models. Fine-aerosol viral RNA was also positively associated with having influenza vaccination for both the current and prior season. NP swab viral RNA was positively associated with upper respiratory symptoms and negatively associated with age but was not significantly associated with fine- or coarse-aerosol viral RNA or their predictors. Sneezing was rare, and sneezing and coughing were not necessary for infectious aerosol generation. Our observations suggest that influenza infection in the upper and lower airways are compartmentalized and independent.

The association of current and prior year vaccination with increased shedding of influenza A might lead one to speculate that certain types of prior immunity promote lung inflammation, airway closure, and aerosol generation. This first observation of the phenomenon needs confirmation. If confirmed, this observation, together with recent literature suggesting reduced protection with annual vaccination, would have implications for influenza vaccination recommendations and policies.

___________  (Please read entire article here by James Lyons Weiler)

Letter to ethical MD’s (snippets below):

The last time the flu vaccine was 60-70% effective was eight years ago.


“This is the CDC’s data  Clearly, Gupta’s “Years” is, in immunological memory, a singular “Year”. Only once out of the last 14 years was the flu vaccine above 59% – that the value was not 60-70%, it was 60%.

This type of misrepresentation is a consistent penchant within the media and of course from the CDC to exaggerate and highly emphasize only positive views and diminish, dismiss, or ignore any negative views on the safety and efficacy of vaccines.

The Jury is In: The Flu Vaccine Reduces its Own Efficacy

Too many studies now exist that have independently come to the same conclusion: increases in the uptake of flu vaccine reduces that vaccine’s effectiveness in the following year – and some studies show the negative effects of mass influenza vaccination last two years.

The studies reporting those results are reviewed in my article, “Diseases with Unknown Etiology Trace Back to Mass Vaccination Against Influenza in 1976“, and they are extensive and damning.

Patients have a right to know the specific nature of their infections, and survivors in families of those who die from respiratory infections deserve an accurate cause of death. Coroners should certainly be required to provide an accurate cause of death in so-called “flu” mortalities. Health departments should be required to count only deaths due to confirmed influenza infection as “flu” – otherwise their numbers perpetuate misperception on the risk of influenza infection, and cause fear leading to increased vaccination. How is this seen as a good thing? The population deserves good and honest doctors and stewards of public health.

HHS could demand swab results for all suspected cases of “flu deaths” with a press release and enforce them with random audits. This annual ritual of fear-mongering over “flu-deaths” hides the fact that as long as thimerosal is injected into patients, they are at increased risk of other infections. And due to heterologous immunity, even without thimerosal, flu vaccines can confuse the immune system and muddle up ineffective immune response by trying to re-purpose B-cells trained on the wrong virus, hobbling the immune system making it unresponsive to similar viruses. Such as next year’s flu strain.

We do need objectivity to arise immediately throughout the public health system in the US, starting with HHS, then to CDC and to all Health Departments around the country. Many studies have also found problems with Tamiflu. But no emergency epidemiological study is addressing the question – why are so many young people dying from “flu”? Many of the reports I’ve seen include mention that they person had not only been vaccinated, they also had taken Tamiflu. And many had taken Tylenol. It’s time to ask the tough questions. The science is there on problems with Tylenol for vaccine-induced fever, and it must be taken into consideration. Fever due to respiratory infections after flu vaccination is still vaccine-induced.

A look at the issues with Tamiflu (see primary scientific literature reviewed here) shows that we cannot ignore the possibility that the human immune system is not infinitely resilient, and that medicine’s approaches to tackling “the flu” is imprecise, not evidence-based, and self-defeating. I’m not talking about the number of antigens the human body can take; I’m talking about the amount of tweaking it can tolerate, especially given the aluminum-dense childhood vaccination schedule. The allopathic medical community would do very well to heed the studies that show that Vitamin D helps alleviate both vaccine injury and severity of viral infections. It helps resolve the unfolded protein response without killing the cells. And the science of ER stress (endoplasmic reticulum stress) shows that Thimerosal is, after all, not safe for human use. Same for aluminum.

Real Reform is Coming – It’s a Mathematical Certainty

Vaccines injure people every day, and kill people every week. Each injury and death informs family members, co-workers, and schoolmates. The flaws in vaccines, combined with misinformation campaigns on safety, fuel the fire and build the vaccine risk aware army. It’s a peaceful army, filled with individuals who are hurt so badly, they do not want others to suffer the same fate. They are altruistic. And under informed, ethical and distributed leadership, they are finding their momentum.

Vaccine safety science reform means removing those in the CDC and HHS that perpetuated the debacle as it grew to proportions that even they could no longer easily deny it. And that’s fine. Let them go. There are many excellent professionals capable of replacing them – people who have not been involved in cooking studies to alter the public’s perception of vaccine risk. People who have withstood unwarranted and unfair criticism by those who live in cowardice of reality. People who now no longer afraid to publish their views. An important question is who among my colleagues in Academic Public Health, and which doctors in Pediatric medicine are willing to #bebrave and take on a debacle as huge as a failed national immunization program? Who will stand up to the AAP and tell them they are wrong?

If you are that type of doctor, it will be easier if you trust those who have worked at this for years. Read Dr. Paul Thomas’ book, The Vaccine Friendly Plan. After the resignations, have him come and teach the entire CDC and HHS what he knows. Consider Dr. Alvin Moss’s wisdom – ask him to create a Conflicts of Interest Policy for CDC and HHS, as he has done for the rest of academic medicine. Bring in Dr. Bob Sears from California, who was willing to stare down threats of the loss of his license to practice medicine because he dared to continue to practice medicine in the face of wanton misinformation and pressure from the AAP. Consider Dr. Richard Frye, and Dr. Chris Exley from the UK, who care first and foremost about the truths that impact total health. Dr. Frye would be great as the new NIH Director, in my opinion. Let these people form a new national public health direction that overrides existing contracts. There are others. Like Dr. Judy Mikovits whose character stands much taller than those who tried – and failed – to silence her – on the issue of adventitious agents in viral vaccines (specifically and quite problematic: retroviruses). Ask Dr. Ted Fogarty about Ethical Vaccinomics, and testing for vaccine injuries. Bring in Dr. John Piesse from Australia and end his persecution there, and put his good will toward safety to work here. We would be lucky to have him.

Create a Manhattan Project focused on reducing vaccine injuries, not on making currently licensed vaccines safer. They are old, and stale, and tired, and they, too, need to go. Bring in exciting new developments in artificial immunization like microneedle patches. Bring in Dr. Kanduc to screen epitopes that are unsafe. Drop aluminum, as many have now called for, and bring in calcium carbonate – if needed at all. Let those pharmaceutical companies who created the disaster make good on their promises to stop making their vaccines. Then we will see new approaches to artificial immunization that compete on the platform of safety.

Don’t just end COIs at ACIP: End ACIP. Create a Vaccine Safety Commission that enforces Science Integrity. Open up the markets. Let ideas thrive. Let consumers choose. Let the FDA do its job. Let the people’s experiences be heard. Establish a paradigm in which the end consumer has a say in the quality of the product. Strip the CDC of the ability to hold patents. End the CDC Foundation. End the differences between drugs and biologics and require randomized clinical trials – with proper placebos, not aluminum hydroxide – for vaccines. Repeal the 1986 Act that protects drug companies from liability for faulty vaccines. Perform random spot checks of vaccines in practices for contamination. The total sum of policies in the National Immunization Program, and the burden of morbidity on the population is a serious threat to our National Security.

Let some new faces and voices drive this reform. Bring in Dr. Dan Neides who had to escape the Cleveland Clinic after speaking his conscience. Let him oversee the transition. Bring in Dr. Brian Hooker to personally issue the pink slips to those who must now go from the CDC. Let all of those named here share his or her experience with Congress. Have Dr. Thompson testify. We need truth and reconciliation. And we need it 42 years ago.

There are MDs who sit in the shadows, silent, and afraid of job loss, sanction, ridicule. Step up. Let your views be known to the current Administration. Join Physicians for Informed Consent. You are not alone. You can help be part of the solution. Attend Health Department meetings and speak up for Informed Consent. Speak up for vaccine exclusions for kids in homes with high lead levels. Speak up for spacing out vaccines and skipping them. Speak up for tolerance and understanding of the pain and anguish parents of kids with autism experience when they are told it’s genetic, they know it’s environmental, and they are told they have to vaccinate their other babies. Speak up against calling CPS for parents who want to take the time they have under the law to consider vaccinations. And, of course, do right by your patients. Listen to their concerns. Inform them of both risks and benefits, as required by Federal Regulations. Let them know they are enrolling themselves or their children (and unborn baby) in post-licensure vaccine safety clinical trials (as required by Federal Regulations). Provide medical and philosophical exemptions for school waivers as required by the laws of your state and the rule of your own conscience. The AAP does not represent the rights and will of the people of the United States of America. Our legislation does.

Let’s aim to not make 2020 vaccination look anything like 2019. We have solutions. We’re now aiming for Healthy People 2050, and the current vaccines have very little to do with our vision. By the way, these ideas don’t come (exclusively) from me. They are shared by hundreds of thousands of American citizens, many of whom have been made sick or lost loved ones to vaccines. #werenotgoingaway #releasetheothermemos #hearthiswell #notmine #Vaxxed #cdctruth #saveourbabies #bebrave #ipak #cdcwhistleblower #rfkcommission #educatebeforeyouvaccinate #vaxxed #learntherisk #wedid #cdclied #stopmandatoryvaccination #learntherisk.”



More just keeps popping out of Pandora’s Box regarding vaccines.

This recent talk shows how vaccines are causing Lyme/MSIDS patients to relapse as well as worsen:  Scottish doctor treating a number of young women who fell ill after their HPV vaccination, which seems to have stimulated a latent Lyme infection to reactivate.  Asymptomatic girls after receiving Gardasil activated dormant Bartonella which was confirmed by testing.

Great video on the flu vaccine’s ineffectiveness:

I could go on and on to infinity.  Something must be done.  Be a part of the solution.







Understanding Q Fever Risk to Minnesotans

Understanding Q Fever Risk to Humans in Minnesota Through the Analysis of Spatiotemporal Trends

Alvarez Julio, Whitten Tory, Branscum Adam J., Garcia-Seco Teresa, Bender Jeff B., Scheftel Joni, and Perez Andres. Vector-Borne and Zoonotic Diseases. February 2018, 18(2): 89-95.  Published in Volume: 18 Issue 2: February 1, 2018

Understanding Q Fever Risk to Humans in Minnesota Through the Analysis of Spatiotemporal Trends

Q fever is a widely distributed, yet, neglected zoonotic disease, for which domestic ruminants are considered the main reservoirs in some countries. There are still many gaps in our knowledge of its epidemiology, and the source of sporadic cases is often not determined. In this study, we show how Q fever surveillance data in combination with information routinely collected by government agencies in Minnesota during 1997 to 2015 can be used to characterize patterns of occurrence of Q fever illnesses and detect variables potentially associated with increased human illness. Cluster analysis and Bayesian spatial regression modeling revealed the presence of areas in Southern Minnesota at higher risk of Q fever. The number of sheep flocks at the county level helped to explain the observed number of human cases, while no association with the cattle or goat population was observed. Our results provide information about the heterogeneous spatial distribution of risk of Q fever in Minnesota.


1280px-Coxiella_burnetii_01Image credit: en:Rocky Mountain Laboratories, NIAID, NIH


The causative agent of Q Fever, Coxiella burnetii, is a small Gram-negative bacterium morphologically similar to Rickettsia, but with genetic and physiological differences.  It has been isolated from approximately 40 species of ticks with possible tick borne transmission reported.  The most common mode of transmission is inhalation of infectious aerosols from fluids of infected animals.  It can become airborne and travel for miles causing outbreaks.  Person to person transmission is possible as well. It can survive standard disinfectants, and is resistant to many other environmental changes like those presented in the phagolysosome.  The CDC reports that 60% of cases are in patients without livestock contact (CDC unpublished data, 2010) and the need for health-care professionals to consider Q fever in the differential diagnosis in patients with a compatible illness, even in the absence of occupational risk or history of direct contact with animal reservoirs.

Supposedly, he United States ended its biological warfare program in 1969. When it did, C. burnetii was one of seven agents it had standardized as biological weapons.

Q Fever can cause acute or chronic illness.
Excellent video by Alicia Anderson, DVM, MPH on new CDC guidelines for Q Fever

Excerpts below:

Summary of Acute Q Fever
Prolonged fever (>10 days) with a normal leukocyte count, thrombocytopenia, and increased liver enzymes is suggestive of acute Q fever infection.
Children with Q fever generally have a milder acute illness than adults.
Children are more likely to have a rash than adults. Rash has been reported in up to 50% of children with acute Q fever.
Women infected with Q fever during pregnancy are at increased risk for miscarriage and preterm delivery.
Women of child-bearing age who receive a diagnosis of Q fever can benefit from pregnancy screening and counseling to guide health-care management decisions

Treatment: Symptomatic patients with confirmed or suspected acute Q fever, including children with severe infections, should be treated with doxycycline, which is most effective if given within the first 3 days of symptoms.  Other antibiotic regimens that can be used if doxycycline is contraindicated because of allergies include moxifloxacin, clarithromycin, trimethoprim/sulfamethoxazole, and rifampin.  Patients with acute Q fever should undergo a careful clinical assessment to determine whether they might be at risk for progression to chronic Q fever because patients at high risk require closer observation during the convalescent period.

Summary of Chronic Q Fever
Persons who are at high risk for development of chronic Q fever include persons with preexisting valvular heart disease, vascular grafts, or arterial aneurysms.
Infection during pregnancy and immunosuppression (e.g., from chemotherapy) are both conditions that have been linked to chronic Q fever development.
Endocarditis and infections of aneurysms or vascular prostheses are the most common forms of chronic Q fever and generally are fatal if untreated.
Chronic Q fever is rarely reported in children.
In contrast with adults, osteomyelitis is one of the most common findings in children with pediatric chronic Q fever.

Treatment:  Adults who receive a diagnosis of chronic Q fever should receive a treatment regimen of doxycycline and hydroxychloroquine (100 mg of doxycycline twice daily with 200 mg of hydroxychloroquine three times daily); duration of treatment might vary by the site of infection. A combination regimen is necessary to eradicate the organism because hydroxychloroquine raises the pH in the acidified phagosomal compartment and, in combination with doxycycline, has been shown to have in vitro bactericidal activity against C. burnetii. Because of potential retinal toxicity from long-term use of hydroxychloroquine, a baseline ophthalmic examination should be performed before treatment and every 6 months thereafter. Both doxycycline and hydroxychloroquine can cause photohypersensitivity, and hypersensitivity to sunlight is a potential complication with acute and chronic treatment regimens. Hydroxychloroquine is contraindicated in persons with glucose-6-phosphate dehydrogenase deficiency and persons with retinal or visual field deficits.

During treatment for chronic Q fever, patients should receive monthly serologic testing for C. burnetii phase I and II IgG and IgM antibodies and monthly clinical evaluations. If an appropriate treatment response is not achieved, monthly monitoring for hydroxychloroquine plasma levels (which should be maintained at 0.8–1.2 µg/mL) and doxycycline plasma levels (which should be maintained at ≥5 µg/mL) should also be performed during the treatment (145,146). Treatment should continue for at least 18 months for native valve infections and at least 24 months for prosthetic valve infections.

Rather than rely on indiscriminate application of predetermined cutoff titers, health-care providers should use serologic testing as a tool to ensure that the phase I IgG is decreasing during treatment in conjunction with recovery from clinical symptoms. A patient who has been treated appropriately for ≥18 months and has recovered from clinical symptoms but whose phase I IgG remains ≥1:1024 might not benefit from continued treatment.

See CDC link for treatment for pregnant women and children.

Q Fever is a notifiable disease in the U.S.