Borrelia mayonii

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Borrelia mayonii
Scientific classification edit
Domain: Bacteria
Phylum: Spirochaetes
Order: Spirochaetales
Family: Spirochaetaceae
Genus: Borrelia
B. mayonii
Binomial name
Borrelia mayonii
Pritt et. al 2016

Borrelia mayonii is a Gram-negative, host-associated spirochete that is capable of causing Lyme disease.[1][2] This organism can infect various vertebrate and invertebrate hosts such as humans and ticks, primarily Ixodes scapularis.[2][3] Migratory songbirds play a role in the dispersal of the tick vector, Ixodes scapularis, across long distances, indirectly dispersing Borrelia mayonii as well.[4]

Phylogenetic information[edit]

Borrelia mayonii was identified as a sensu lato (broad sense), genospecies (Bbsl) of the known microbe, Borrelia burgdorferi.[5] A genospecies is a cluster of organisms with similar core genes that usually does not undergo genetic recombination with diverged organisms.[6]  Two isolates, gene strains, of B. mayonii, named MN14-1420 and MN14-1539, were sequenced, process of arranging a chain of genetic information to match up to a specific organism's genetic code, and compared to the genome or genetic material of Borrelia burgdorferi.[5] With a nucleotide similarity of 93.83% in the linear chromosome compared to other known genospecies, B. mayonii can be considered a new genospecies (Bbsl).[5]


Borrelia mayonii is a bacterial genospecies discovered in the Midwestern United States[5] by Pritt and colleagues at the Mayo Clinic in Minnesota during routine polymerase chain reaction (PCR) of the oppA1 gene of B. burgdorferi in 2016.[3] According to Pritt, six samples were atypical and did not resemble any known species. These atypical microorganisms were later named after the Mayo Clinic as a new genospecies. The spirochaete, a flexible and spiral twist bacterium, was also detected in the blood of infected individuals using PCR and microscopy and was cultivated or grown in a modified Barbour-Stoenner-Kelly (BSK) plate, a microbial growth plate consisting of bovine serum albumin and rabbit serum,[7] at 34°C under oxygen levels lower than that of normal atmospheric conditions, centrifuged at 8000 X g for 10 minutes, isolated using Qiagen DNA kit, and washed using dH2O.[5]

This genospecies has the potential to cause Lyme disease (Lyme borreliosis).[3]


The B. mayonii genome is about 1.31 megabase pairs (Mbp) with an average 26.9% GC (guanine and cytosine) content.[5] It has a linear chromosome with an additional 15 plasmids, eight linear and seven circular.[5] The genomes of the two isolates have similar plasmids seen in Borrelia burgdorferi. The MN14-1420 isolate have a vls locus, a specific position on a chromosome, consisting of 24 silent cassettes, a mobile gene that floats around.[5] B. burgdorferi has 15 silent cassettes with a vlsE expression site.[8] The vls locus with the vlsE site, as it is present in strain B. burgdorferi B31, encodes a lipoprotein, a fatty protein, that allows B. burgdorferi to infect various mammalian hosts.[8][9] B. mayonii may also use this locus as a mechanism of evading host immune system. However, the isolates lack various genomic regions seen in B. burgdorferi such as the region that codes for CspZ (complement inhibitor) and BB_K32 (fibronectin binding protein).[5]


Since this organism is an obligate parasite, its metabolism outside of the host is unclear. However, B. mayonii has genes for purine salvage, a type of nucleotide salvage, and metabolism, but its use of these genes is unknown.[5] According to Integrated Microbial Genomes System, this parasite has genes that allow this organism to synthesize various amino acids such as L-alanine, L-glutamate, glycine, L-asparagine, and L-glutamine.[10]


Infection by B. mayonii is also transferred from the bite of Ixodes scapularis, a tick.[11] B. mayonii causes Lyme disease like B. burgdorferi, with the symptoms of fever, headache, rash, neck pain, and arthritis. However, B. mayonii also has additional symptoms differentiating it from B. burgdorferi, such as nausea, vomiting, macular rash, and neurological symptoms.[3] To identify infection with B. mayonii, blood smears, slides with blood samples on them for use with a microscope,[12] may be used. Mayonii spirochetes in blood smears indicate a positive infection for Lyme disease caused by B. mayonii.[12] Another alternative is using Lyme disease PCR tests, which is currently only available at the Mayo Clinic.[12] To treat this infection in early stages, the current drug of choice is doxycycline, an antibiotic, over a 2- to 4-week course.[12]

In later stages, addressing treatment of both cyst and adult stages of the organism at the same time so as to prevent relapse may be helpful.[13][14] Spirochetes in the Borrelia family may enter cyst form in unfavorable conditions and "reappear" in "L" (larval) form as conditions become suitable, advancing into adult spirocheteal forms. "These various atypical forms were suggested to be part of a complex developmental cycle, a form of resistance to adverse conditions, and a source for reproduction under more favorable conditions. Reconversion of cystic Borrelia burgdorferi into the typical spiral form has been demonstrated in vitro and in vivo."[15]


  1. ^ Margulis, L.; Ashen, J. B.; Sole, M.; Guerrero, R. (1 August 1993). "Composite, large spirochetes from microbial mats: spirochete structure review". Proceedings of the National Academy of Sciences. 90 (15): 6966–6970. Bibcode:1993PNAS...90.6966M. doi:10.1073/pnas.90.15.6966. PMC 47056. PMID 8346204.
  2. ^ a b Barbour, AG; Hayes, SF (December 1986). "Biology of Borrelia species". Microbiological Reviews. 50 (4): 381–400. doi:10.1128/MMBR.50.4.381-400.1986. PMC 373079. PMID 3540570.
  3. ^ a b c d Pritt, Bobbi S; Mead, Paul S; Johnson, Diep K Hoang; Neitzel, David F; Respicio-Kingry, Laurel B; Davis, Jeffrey P; Schiffman, Elizabeth; Sloan, Lynne M; Schriefer, Martin E; Replogle, Adam J; Paskewitz, Susan M; Ray, Julie A; Bjork, Jenna; Steward, Christopher R; Deedon, Alecia; Lee, Xia; Kingry, Luke C; Miller, Tracy K; Feist, Michelle A; Theel, Elitza S; Patel, Robin; Irish, Cole L; Petersen, Jeannine M (May 2016). "Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study". The Lancet Infectious Diseases. 16 (5): 556–564. doi:10.1016/S1473-3099(15)00464-8. PMC 4975683. PMID 26856777.
  4. ^ Scott, John D.; Anderson, John F.; Durden, Lance A. (February 2012). "Widespread Dispersal of Borrelia burgdorferi–Infected Ticks Collected from Songbirds Across Canada". Journal of Parasitology. 98 (1): 49–59. doi:10.1645/GE-2874.1. PMID 21864130. S2CID 23940100.
  5. ^ a b c d e f g h i j Kingry, Luke C.; Batra, Dhwani; Replogle, Adam; Rowe, Lori A.; Pritt, Bobbi S.; Petersen, Jeannine M.; Brissette, Catherine A. (28 December 2016). "Whole Genome Sequence and Comparative Genomics of the Novel Lyme Borreliosis Causing Pathogen, Borrelia mayonii". PLOS ONE. 11 (12): e0168994. Bibcode:2016PLoSO..1168994K. doi:10.1371/journal.pone.0168994. PMC 5193363. PMID 28030649.
  6. ^ Kumar, Nitin; Lad, Ganesh; Giuntini, Elisa; Kaye, Maria E.; Udomwong, Piyachat; Shamsani, N. Jannah; Young, J. Peter W.; Bailly, Xavier (January 2015). "Bacterial genospecies that are not ecologically coherent: population genomics of". Open Biology. 5 (1): 140133. doi:10.1098/rsob.140133. PMC 4313370. PMID 25589577.
  7. ^ Wang, G.; Iyer, R.; Bittker, S.; Cooper, D.; Small, J.; Wormser, G. P.; Schwartz, I. (21 October 2004). "Variations in Barbour-Stoenner-Kelly Culture Medium Modulate Infectivity and Pathogenicity of Borrelia burgdorferi Clinical Isolates". Infection and Immunity. 72 (11): 6702–6706. doi:10.1128/IAI.72.11.6702-6706.2004. PMC 523011. PMID 15501807.
  8. ^ a b Zhang, JR; Norris, SJ (August 1998). "Genetic variation of the Borrelia burgdorferi gene vlsE involves cassette-specific, segmental gene conversion". Infection and Immunity. 66 (8): 3698–704. doi:10.1128/IAI.66.8.3698-3704.1998. PMC 108404. PMID 9673251.
  9. ^ Norris, Steven J. (10 December 2014). "vls Antigenic Variation Systems of Lyme Disease Borrelia: Eluding Host Immunity through both Random, Segmental Gene Conversion and Framework Heterogeneity". Microbiology Spectrum. 2 (6): 471–489. doi:10.1128/microbiolspec.MDNA3-0038-2014. ISBN 9781555819200. PMC 4480602. PMID 26104445.
  10. ^ "IMG". Retrieved 2017-04-26.
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  12. ^ a b c d "CDC>Ticks Home>Diseases transmitted by ticks>Borrelia mayonii". Retrieved 2017-04-04.
  13. ^ Miklossy, Judith; Kasas, Sandor; Zurn, Anne D; McCall, Sherman; Yu, Sheng; McGeer, Patrick L (25 September 2008). "Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis". Journal of Neuroinflammation. 5: 40. doi:10.1186/1742-2094-5-40. PMC 2564911. PMID 18817547.
  14. ^ Brorson, Øystein; Brorson, Sverre-Henning; Scythes, John; MacAllister, James; Wier, Andrew; Margulis, Lynn (3 November 2009). "Destruction of spirochete Borrelia burgdorferi round-body propagules (RBs) by the antibiotic Tigecycline". Proceedings of the National Academy of Sciences of the United States of America. 106 (44): 18656–18661. Bibcode:2009PNAS..10618656B. doi:10.1073/pnas.0908236106. PMC 2774030. PMID 19843691.
  15. ^ Miklossy, Judith; Kasas, Sandor; Zurn, Anne D; McCall, Sherman; Yu, Sheng; McGeer, Patrick L (25 September 2008). "Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis". Journal of Neuroinflammation. 5: 40. doi:10.1186/1742-2094-5-40. PMC 2564911. PMID 18817547.