Initially, Dr. Benjamin Luft at Stony Brook School of Medicine thought that mapping the genome of Borrelia would allow researchers to develop a treatment and vaccine faster.  He knew it would be a huge undertaking as Borrelia has one-thousand seven-hundred thirty-eight (1738) genes in a DNA strand which makes it the most complex bacteria currently known to man.

The first strain was mapped in 2009, 13 more strains were mapped in 2010 and by 2014 there were 42 stains mapped (35 Lyme related Borrelia and 7 relapsing fever related Borrelia.)

Dr. Luft was quoted in 2010 by as saying, "By characterizing every gene in the Lyme disease MSIDS agents family, we have a blueprint of every possible characteristic of the organism. This is the building block to developing more accurate and effectivee diagnostic tests, therapeutic agents and vaccines."

He continued saying, "We are depositing the millions of nucleotides that we have sequenced in the public database so that this valuable information will help to further enhance our research and that of other Lyme disease MSIDS investigators.”

Dr. Luft and colleagues point out in the study that improved diagnostics are needed because the best clinical sign of Lyme disease MSIDS, the erythema migrans skin rash, does not always occur in patients. In addition, diagnostic assays and vaccines developed before their blueprint of the entire genome of B. burdorferi have had less than satisfactory results.

“A driving force for doing this project was the observation that certain forms of the bacteria can be more invasive than others,” added Dr. Steven E. Schutzer, lead author, and Professor of Medicine, University of Medicine and Dentistry of New Jersey. “We wanted to find out why and how to identify this property.”

As more and more ticks were collected, and strains were being isolated from humans rather than animals or test tubes, alarming facts unfolded.

There were up to a dozen strains of different Borrelia within different ticks which disproved the idea that Borrelia burgdorferi was transmitted by Eastern black-legged ticks (deer ticks) only.

Also, the number of “wild” strains began to snowball as it was discovered that strains adapted to their host, and changed their genetic sequencing to best evade the individual’s immune system and/or antibiotic treatment.

The new estimates placed Lyme disease MSIDS causing Borrelia at over 100 species and over 300 worldwide.

But it wouldn’t be enough to map the genomes of just Borrelia burgdorferi.  Lyme disease MSIDS was soon found to be caused by a number of genus and eventually found in soft-shelled ticks as well:

·        Borrelia burgdorferi sensu stricto  (countless strains of B. burgdorferi)

·        Borrelia afzeli

·        Borrelia garinii

·        Borrelia miyamotoi

·        Borrelia valaisiana

·        Borrelia spielmanii

·        Borrelia bissettii 

·        Borrelia andersonii

·        Borrelia californiensis

·        Borrelia americana

·        Borrelia carolinensis

·        Borrelia kurtenbachii

·        Borrelia hermsii

·        Borrelia turicatae

·        Borrelia coriaciae

In Asia: B. japonica, B. turdi, B. sinica, B. bissettii, B. tanukii, B. yangtze

In Europe: B. lusitaniae, B. bissettii and B. valaisiana, B. spielmanii, B. bavariensis

In Australia and New Zealand: B. burgdorferi, B. garnii found in Ixodes auritulus and Ixodes uriae. NOTE: For more information on Lyme disease in Australia see Australian Lyme Disease Association and

In 2014 Pub Med published the following from authors: Di L, Pagan PE, Packer D, Martin CL, Akther S, Ramrattan G, Mongodin EF, Fraser CM, Schutzer SE, Luft BJ, Casjens SR, Qiu WG.

The bacterial genus Borrelia (phylum Spirochaetes) consists of two groups of pathogens represented respectively by B. burgdorferi, the agent of Lyme borreliosis, and B. hermsii, the agent of tick-borne relapsing fever. The number of publicly available Borrelia genomic sequences is growing rapidly with the discovery and sequencing of Borrelia strains worldwide. There is however a lack of dedicated online databases to facilitate comparative analyses of Borrelia genomes.”

“We have developed BorreliaBase, ( an online database for comparative browsing of Borrelia genomes. The database is currently populated with sequences from 35 genomes of eight Lyme-borreliosis (LB) group Borrelia species and 7 Relapsing-fever (RF) group Borrelia species.”

Major pathogenic species from soft ticks found world-wide



Geographical distribution

Argas monolakensis

Mono Lake virus

Western United States

Ornithodoros capensis

Soldado virus


O. coriaceus

Borrelia coriaciae

Pacific Coast US

O. parkerii

Borrelia parkerii

United States

O. erraticus

Crocidurae Borrelia 
Borrelia hispanica

North Africa 
Iberian Peninsula

O. hermsii

Borrelia hermsii

Western United States

O. moubata

Borrelia duttonii

East and Southern Africa

O. tartakovskyi

Borrelia latyschevi

Central Asia

O. tholozani

Borrelia persica

Israel, Central Asia

O. turicata

Borrelia turicatae

Southwest United States 
Central America

O. savignyi

intense itching 
Virus Alkhurma

Africa, Asia



Relapsing Fever

Once thought to be a co-infection of Lyme disease, relapsing fever is now considered a separate group of Borrelia, and is genetically different enough from the dozens of other Lyme disease species to be given its own designation in the BorreliaBase. These strains are found all around the world.

In the US, relapsing fever is spread by ticks and lice.

The deer tick in the Northeast has been found to transmit Borrelia miyamotoi, which is a type of relapsing fever, and the other forms of relapsing fever are spread by soft ticks, O. parkeri and O.turicatae.

These ticks spread Borrelia hermsii, Borrelia parkerii, Borrelia turicatae, Borrelia crocidurae, Borrelia recurrentis and Borrelia duttonii – 7 strains (including B. miyamotoi) that were completely mapped and documented from tick and human blood samples.

The disease has been found in most every part of the country but especially virulent species live in caves (SPURLUNKERS BEWARE!), and all soft ticks can live over 10 years and will remain infectious throughout their entire life.

Unfortunately, the ticks infect humans very quickly and very rarely does a person even know they were bitten.

Most people who are infected get sick about a week after they are bitten. The main symptom as you may expect is a fever that comes and goes.It can be a very high fever or a moderate fever and may go away for years or show up every week or month at times.

In addition to repeating bouts of fever, chills, headaches, fatigue, malaise, muscle or joint aches, nausea and vomiting.It can also cause conjunctivitis, a dry cough and even anorexia.The symptoms may that last from 2 - 7 days, punctuated by periods of apparent wellness. The initial symptoms are the most severe, with sudden onset of high fever and severe headache. A spotted and/or itchy rash may sometimes occur during this first episode of illness.

The fever cycles often conclude in a classic pattern commonly referred to as first the patient experiences a spike in fever, sometimes up to 106ºF or more, and an increased metabolic rate (such as rapid breathing and tachycardia) is seen. Shortly thereafter, body temperature falls dramatically and the patient endures drenching sweats. Severe drops in blood pressure can occur during this second stage.

These cycles are caused by the ability of spirochetes to shift their outer surface protein coat in order to evade the human immune response; once a new clone is created and the organism multiplies in sufficient numbers, clinical relapses occur.

Liver and spleen involvement are not uncommon in relapsing fever, but seem to occur more frequently in LBRF. Neurologic complications can also occur – again, more commonly in LBRF – and include meningitis, seizures, cranial neuropathies (especially facial palsy) and even coma.

Myocarditis can be a fatal complication of either LBRF or TBRF. Relapsing fever can also cause complications in pregnant women, resulting in spontaneous abortion, premature birth or neonatal death. (See How Lyme/MSIDS Kills)

The Lyme and Tick-borne Diseases Research Center at Columbia University has published the following regarding diagnosis and treatment:

Diagnosis for Relapsing Fever Lyme Disease:

A pattern of recurrent fevers in a patient from an endemic area should prompt an evaluation for relapsing fever. Conventional blood tests may show an increased white blood cell count, low platelets, mildly increased bilirubin, elevated erythrocyte sedimentation rate, and an increase in prothrombin time (PT) and partial thromboplastin time (PTT) coagulation tests, but none of these are diagnostic. Serologic tests (direct and indirect immunofluorescent assays) for relapsing fever can be performed, but they are not standardized across laboratories and not useful for timely diagnosis in any case. Cross reaction with antibodies to Lyme disease and syphilis have also been reported.

PCR tests exist but are not widely available.

The gold standard for relapsing fever diagnosis is the visualization of spirochetes in smears of peripheral blood or cerebrospinal fluid. Dark field microscopy is the preferred method, but various stains (such as Wright-Giemsa or acridine orange) are also frequently employed. The number of circulating spirochetes tends to decrease with each febrile episode.

Treatment for Relapsing Fever Lyme Disease:

Louse-borne relapsing fever is usually treated with a single dose of antibiotic. Antipyretics (aspirin, NSAIDs or acetaminophen) are usually administered concomitantly. First line antibiotic agents are doxycycline and erythromycin, but chloramphenicol and parenteral penicillin G are also used. Treatment for tick-borne relapsing fever utilizes the same antibiotics, but lasts longer, typically one week. A common regimen is 100 mg of doxycycline every 12 hours, or 500 mg of erythromycin every 6 hours, for one week. Intravenous penicillin is recommended in cases of suspected or proven central nervous system involvement.

A common and potentially serious complication of relapsing fever treatment ( similar to other forms of Lyme disease) is the Jarisch-Herxheimer reaction, caused by the massive release of cytokines (primarily TNF-alpha, IL-6 and IL-8) during the spirochete die-off. The reaction usually begins 2-4 hours after antibiotic administration and is similar to the crisis stage of the fever cycle. Typical presentations are elevated fever, increased respiration and heart rate, excessive sweating, chills, and sudden changes in blood pressure. Fatalities from the J-H reaction can occur. Research suggests that administration of anti-TNF-alpha antibodies can ameliorate the severity of the J-H reaction, but aspirin, acetaminophen and corticosteroids are ineffective in doing so.

The mortality rate for untreated LBRF ranges widely but can approach 70%. In TBRF it is on the order of 5-10%. Treated properly, the death rate is reduced to around 1%, but TBRF patients often report residual symptoms even after treatment. These symptoms are usually associated with delayed diagnosis and initiation of treatment.

Due to the lack of study regarding relapsing fever relative to other infectious diseases, it seems quite likely that the same issues will be contentious with respect to persistent symptoms after treatment.

Like other Borrelia species the reasons for spirochetes in Relapsing Fever persisting  in spite of antibiotic treatment are only slowly coming to light.  SEE CHRONIC LYME DISEASE.

There are 850 tick species, and approximately 300 can transmit disease into human hosts. It is no wonder that Lyme is now a world-wide epidemic.



According to, he first and only licensed vaccine against Lyme disease was developed by SmithKline Beecham (now GlaxoSmithKline). Given in a three-dose series, the vaccine had an unusual method of action: it stimulated antibodies that attacked the Lyme bacteria in the tick’s gut as it fed on the human host, before the bacteria were able to enter the body. This was about 78% effective in protecting against Lyme infection after all three doses of the vaccine had been given.

The vaccine, called LYMERix, was licensed in 1998, but withdrawn by 2002 due to concerns regarding the safety of the vaccine.  Stories were spread by media and internet of people who became sick with all of the symptoms of Lyme disease after the vaccination.

In hindsight it is clear that not enough was understood about the disease in 1998 to release a vaccine, although now, with the pressure of the revised CDC numbers of one million new cases of Lyme disease each year, the pressure will continue to mount.  Already there are many promising trials being held with the most likely winner coming from Dr. Luft’s team at Stony Brook.

What makes this vaccine especially powerful is that it works on all North American strains of  Borrelia by triggering a healthy immune response with no major side effects.

The likelihood of a successful vaccine reaching the marketplace in 2015 look better than ever.





Jenna Seaver author of lyme disease resource

Jenna in Maui



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