Pathogens 2019, 8(3), 117;


Babesia microtiBorrelia burgdorferi Coinfection

Rutgers New Jersey Medical School, Department of Microbiology, Biochemistry and Molecular Genetics, Newark, NJ 07103, USA
*Authors to whom correspondence should be addressed.
Received: 15 May 2019 / Accepted: 26 July 2019 / Published: 31 July 2019


The incidence and geographic distribution of human babesiosis is growing in the U.S. Its major causative agent is the protozoan parasite, Babesia microti. B. microtiis transmitted to humans primarily through the bite ofIxodes scapularis ticks, which are vectors for a number of other pathogens. Other routes of B. microti transmission are blood transfusion and in rare cases of mother-to-foetus transmission, through the placenta. This review discusses the current literature on mammalian coinfection with B. microtiand Borrelia burgdorferi, the causative agent Lyme disease.
Please see above link for entire study.  Highlights:
  • B. microti and Borrelia burgdorferi coinfection is common in vector (ticks) & host (animals & humans)
  • In endemic regions, almost 20% of Lyme disease patients reported concurrent babesiosis while up to 25% of babesiosis patients also had Lyme disease
  • A large percentage of patients with chronic/post-treatment Lyme disease syndrome (52%) show evidence of past or active Babesia coinfection
  • There is some evidence that coinfections with a different Babesia species, B. duncani, and B. Burgdorferi may be more common than previously suspected.
  • Of the two studies that have examined B. microtiB. burgdorferi coinfection on humans both studies found patients reported symptoms of greater variety and longer duration than those infected with Bb alone
  • In C3H mice, B. microti coinfection exacerbates symptoms of arthritis caused by B. burgdorferi because B. microti causes splenic dysfunction that reduces B- and T-cell function and the production of antibodies required to control Bb infection
  • It aptly points out that besides infected ticks, humans can become infected with Babesia congenitally as well as by blood transfusions.

Recently these two articles essentially found divergent outcomes. This article shows Babesia is widespread in Canada, while this one states it’s rare:

The only conclusion that can be made is that blood testing is not picking it up. I’ve read over and over that Babesia is rarely detected using one diagnostic test alone.

Yet, if I am reading this properly, they only used one test. If a sample was reactive, only then did they test it further – kind of like using 2-tiered testing for Lyme when you only move onto the Western Blot IF you test positive first using the Elisa. So these patient samples were tested only once at the beginning to determine who had reactive samples to Babesia.

This testing discrepancy that differs from reality is true for all tick-borne diseases and practitioners need to become educated in this fact as well as understand the importance of symptomology to determine a clinical diagnosis. The continued stubbornness of utilizing poor testing to weed out people in the beginning is foolish. It only seems logical to cast a wider net in the beginning rather than a narrower one. Everyone knows testing is abysmal, yet it’s followed like the Pied Piper to the doom of patients.

People are going to continue to fly under the radar with these pathogens until better testing is developed. Mainstream medicine has been lobotomized and is functioning without the capacity of a brain.


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