Amblyomma americanum (Acari: Ixodidae) Ticks Are Not Vectors of the Lyme Disease Agent, Borrelia burgdorferi (Spirocheatales: Spirochaetaceae): A Review of the Evidence

Ellen Y Stromdahl, Robyn M Nadolny, Graham J Hickling, Sarah A Hamer, Nicholas H Ogden, Cory Casal, Garrett A Heck, Jennifer A Gibbons, Taylor F Cremeans. Mark A Pilgard
Journal of Medical Entomology, online first 31 January 2018.


In the early 1980s, Ixodes spp. ticks were implicated as the key North American vectors of Borrelia burgdorferi (Johnson, Schmid, Hyde, Steigerwalt and Brenner) (Spirocheatales: Spirochaetaceae), the etiological agent of Lyme disease. Concurrently, other human-biting tick species were investigated as potential B. burgdorferi vectors.

Rashes thought to be erythema migrans were observed in patients bitten by Amblyomma americium (L.) (Acari: Ixodidae) ticks, and spirochetes were visualized in a small percentage of A. americanum using fluorescent antibody staining methods, sparking interest in this species as a candidate vector of B. burgdorferi. Using molecular methods, the spirochetes were subsequently described as Borrelia lonestari sp. nov. (Spirocheatales: Spirochaetaceae), a transovarially transmitted relapsing fever Borrelia of uncertain clinical significance.

In total, 54 surveys from more than 35 research groups, involving more than 52,000 ticks, have revealed a low prevalence of B. lonestari, and scarce B. burgdorferi, in A. americanum. In Lyme disease-endemic areas, A. americanum commonly feeds on B. burgdorferi-infected hosts; the extremely low prevalence of B. burgdorferi in this tick results from a saliva barrier to acquiring infection from infected hosts.

At least nine transmission experiments involving B. burgdorferi in A. americanum have failed to demonstrate vector competency. Advancements in molecular analysis strongly suggest that initial reports of B. burgdorferi in A. americanum across many states were misidentified B. lonestari, or DNA contamination, yet the early reports continue to be cited without regard to the later clarifying studies.

In this article, the surveillance and vector competency studies of B. burgdorferi in A. americanum are reviewed, and we conclude that A. americanum is not a vector of B. burgdorferi.



All I can say is something’s happening in the South that’s causing the same symptoms as Lyme in nouthern patients.  Also, a review of old studies does not necessarily mean a thing is or is not.  It’s just a review of old studies.  Garbage in, garbage out, as they say.

I’m certainly no entomologist; however, I read over and over how difficult it is to study borrelia in a lab setting.  It’s impossible to grow & measure.

A great quote here: “If you look at major medical microbiology and infectious disease textbooks, they state that after 4 weeks you can’t find the Lyme bacteria anymore. Therefore Lyme is then categorised as ‘post infectious’. But I get back to the point I’ve made before: if you can’t culture it, you cannot know anything about its viability. You do not have a organism specific test (culture or PCR), that guides your ‘test of cure’. How do you say that a bacteria is killed, when you couldn’t grow and measure it in the first place?” “One of the rules of infectious diseases medicine is that once you stop treatment and the patient stays better, they are cured. When they get worse, the infection has returned and they have relapse of infection and need repeat treatment. My ID colleagues live by that rule with most other infections, but not with Lyme.”

And again, Dr. Masters fought tooth and nail to get Lyme or a Lyme-like illness recognized in his southern patients:  Masters worked with Missouri entomologist, Dorothy Fier, who found borrelia in 2% of sampled lone star ticks and who supported Masters’ Missouri Lyme. Despite publicity and validation, the CDC insisted that the EM rash was NOT diagnostic for LD for Missouri patients due to the fact that neither Ixodes dammini nor Ixodes pacificus were found there. Go here: for a great article on how Andrew Spielman’s tick maps ruled Lyme Land like the iron curtain, and frankly still do, dictating where Lyme is and is not. (nothing’s changed)   Part 4: The CDC essentially tried blackmailing Masters into signing off on the study before they would let him see the final draft. Refusing the bait, he published a letter of objection in the Journal of Infectious Diseases as well as an article of his own in Missouri Medicine which showed Missouri patients met the CDC surveillance definition for LD and growing evidence that lone star ticks were infected with an unidentified spirochete causing identical symptoms of LD in patients. When the CDC study came out they unbelievably attributed the rashes they labeled STARI to an allergy to tick saliva! In the acknowledgment section of the paper where dozens of folks were thanked, they completely omitted the man who made it all possible – Dr. Ed Masters.  Supporting Masters’ theory, James H. Oliver, Jr., Callaway later showed that mice from 5 southern states tested positive for Borrelia burgdorferi, the causative agent of LD and had just as many reactive antibodies as mice from Connecticut. He also found a range of new Southern ticks transmitting a literal hodgepodge of borrelia as well as a unique Southern strain of Bb with unusual outer surface proteins that are undetectable on Northern blood tests.
This was over 20 years ago and Southern authorities and the CDC still deny Lyme: They also still cling to the contention that STARI is a rash-only illness unrelated to Lyme and that antibiotics should be used sparingly if at all. Masters’ patients all improved dramatically with longer antibiotic treatment.
Left out in the links above but on page 185 in Weintraub’s book she reveals another fly in the ointment: The CDC kept changing the blood tests from year to year until samples that were positive were now negative.

No, my friends, I definitely smell a skunk.

I say, “Keep looking!”