I refer those who persist in making analogies between Lyme disease and tick relapsing fever to this reference which clearly distinguishes between both diseases ( http://www.cdc.gov/relapsing-fever/
I don't find that to be the best link on the CDC site for making comparisons between Lyme disease and relapsing fever. This page is more appropriate for that purpose:
Vector Interactions and Molecular Adaptations of Lyme Disease and Relapsing Fever Spirochetes Associated with Transmission by Ticks
http://wwwnc.cdc.gov/eid/article/8/2/01 ... rticle.htm
I don't see why one wouldn't immediately want to make comparisons - they're their closest relative, genetically speaking, and have more similarities to each other than to Treponema.
Here's the section on species comparisons:
From the observations reviewed above, one phenomenon shared by B. burgdorferi and B. hermsii is the synthesis of OspC and Vsp33 at the time these spirochetes are transmitted by tick bite. DNA and amino acid sequence analysis also shows that these proteins are homologous (51) and that antisera produced to the two proteins are cross-reactive (51–53). Several other species of Borrelia also contain a related gene or protein recognized with either Northern or Western blot (53). Therefore, this family of surface proteins may be shared by all species of borreliae, which are spirochetes defined, in part, by their requirement for an arthropod vector for transmission. Our hypothesis is that these proteins are involved in the transmission of these spirochetes from tick to vertebrate host.
The temporal synthesis of OspC and Vsp33 during spirochete infection in ticks is strikingly different between B. burgdorferi and B. hermsii, but appears to be adaptive to ixodid versus argasid ticks, which have considerably different feeding behaviors. Most nymphal I. scapularis take 3 to 4 days to feed whereas O. hermsi feed to repletion in only 15 to 90 minutes. In free-living, unfed I. scapularis, B. burgdorferi is usually found only in the midgut and OspC is not expressed. However, following tick attachment B. burgdorferi replicates, downregulates OspA, disseminates from the midgut to salivary glands, synthesizes OspC, and is transmitted via the saliva after 2 to 4 days of feeding.
An increase in temperature and the ingestion of blood, environmental cues associated with a free-living tick having attached and begun to feed on a host, stimulate a subpopulation of B. burgdorferi to transiently synthesize OspC during feeding. If OspC is required for transmission of B. burgdorferi by tick bite, there is ample time, because of the slow feeding behavior of Ixodes ticks, for both the dissemination of spirochetes from the midgut to the salivary glands and the novel synthesis of OspC. Numerous studies have shown that humans and experimental animals infected by tick bite seroconvert to OspC early, demonstrating that this protein is expressed in mammals for some undetermined period.
In free-living, unfed O. hermsii, the distribution of B. hermsii in these ticks and their expression of Vsp33 are just the opposite, with spirochetes established in the salivary glands and nearly all expressing Vsp33. In the scenario with O. hermsi feeding for only minutes after encountering a host, there is no time for spirochetes to disseminate out of the midgut, penetrate the salivary glands to the salivary duct, and also synthesize a new Osp that may facilitate (or be required for) transmission. Hence B. hermsii is in a constant state of readiness for transmission that is comparable to the phenotype and localization displayed by B. burgdorferi only briefly during a few days of attachment by I. scapularis (Figure 4).
The phenotypic changes and dissemination shown by B. burgdorferi during transmission by tick bite point to several possible functions for OspC: dissemination from the midgut, infection of the salivary glands, or successful colonization in the mammal following delivery into the feeding lesion in the dermis. Because the changes in protein synthesis and movement of the spirochetes occur rapidly in the nymphal ticks, identifying the precise time when OspC is produced in relation to the spirochetes’ movement in the tick is difficult to determine by microscopy. Quantitative reverse transcription-PCR may help increase sensitivity through detecting specific gene transcripts in different tick tissues sampled a different times. However, the events shown by B. hermsii during its dissemination in the tick are much more protracted and may shed some light on the function of OspC, Vsp33, or other proteins.
Because it takes approximately 3 weeks or more for B. hermsii to disseminate and become established in the salivary glands of O. hermsi, immunofluorescent staining of these spirochetes in tick tissues at successive intervals after infection has recently shown that B. hermsii can infect the salivary glands before the upregulation of Vsp33. At least for this relapsing fever spirochete, Vsp33 does not appear to be needed either for dissemination from the gut or invasion of the salivary glands.
Additional species of Borrelia and their expression of Osps associated with transmission need to be examined. If the OspC, Vsp33, or other proteins are required for transmission by ticks, we anticipate finding homologs to these proteins in other species associated with their transmission. Other relapsing fever spirochetes in Ornithodoros ticks, B. anserina in Argas ticks, and other borrelia associated with ixodid ticks will be fruitful tick-spirochete associations to study. A comparison of borrelial genomes will also be helpful when such sequences become available. Finally, with important advances being made recently to inactivate and introduce genes in these spirochetes (54,55), experiments to examine the importance of specific proteins in various steps of the transmission cycle are on the horizon.
Where there are unanswered questions - for me at least - are the relapsing fever spirochetes which are NOT in Ornithodoros ticks but now found in hard bodied ticks including Ixodes
ticks. What role do they play in tick-spirochete associations? Where are they found throughout the tick's body? How quickly do they disseminate into salivary glands or are they there most of the time? I simply don't know, but I think this is something important to know for disease transmission purposes.
Incidentally, relapsing tick fever is easily cured by a short course of oral antibiotics; it is characterized by a pattern of 3-4 cycles that occurs at regular -- not irregular-- seven day intervals -- and then, no more (most likely because immunity develops). Some forms of late syphilis can be cured by penicillin . Most likely, this erroneous concept of "relapsing Lyme disease" was taken from the cancer literature.
I know about the fast repetitive cycles where relapsing fever shows up in the blood. But does it always happen that the infection is cleared or can it be latent? I thought I'd already cited literature here which provided evidence it can be latent in the mammalian host and it is unknown how often this occurs.
Why do you think Dr. Ben Luft is mischaracterizing Lyme disease as a relapsing disease? He is a key researcher of Lyme disease and its variability. Why would he draw from cancer literature to make such an association (and where, if you can be more precise - how is Borrelia similar to cancer, because I've never heard of this conceptual link you're making?)
Isn't there some evidence Lyme disease does relapse, but on a slower timescale than relapsing fever spirochetes found in soft bodied ticks? Aren't there at least two recorded bacterial peaks in early infection with Lyme disease recorded - one at week 5, then another around week 9-10? Or would you not consider these peaks to be relapses?
What about its antigenic variation cycles throughout infection? I would consider their similarity in antigenic variation cycles to be a good comparison - even if the genetic mechanism behind how RF spirochetes do it differs from the mechanism for how LD spirochetes do it.
Comparing Lyme disease to syphilis is also hazardous and inappropriate. Although both diseases are caused by spirochetes, the pathology is very different; that is the major reason why Treponema pallidum -- the spirochete that causes syphilis -- is placed in a different GENUS than Borrelia burgdorferi. The genetic relationship of T. pallidum is closer to T. denticola than to B. burgdorferi; although T. denticola is a common inhabitant of the oral cavity and is one of the agents involved in gingivitis, it doesn't cause syphilis. So, forget all of these stupid analogies that only serve to "muddy the waters" and cause more confusion.
Pathology is different, genetically different in a number of ways - agreed. Here's a good ref for anyone interested:
Comparative Genome Analysis of the Pathogenic Spirochetes Borrelia burgdorferi and Treponema pallidum
I particularly find this passage from the above paper to be fascinating, regarding hortizontal gene transfer from other bacteria (archaea) and also (!) eukaryotes:
In spite of the high level of conservation in the translation apparatus, we did detect a few interesting examples of evolutionary divergence between the two species. One notable case was the prolyl-tRNA synthetase from B. burgdorferi, where phylogenetic analysis strongly suggested that the enzyme in B. burgdorferi has been acquired from a eukaryotic source by the xenologous displacement mechanism (78). The other aminoacyl-tRNA synthetases are strongly conserved between the spirochetes, but phylogenetic analysis provided evidence for likely ancient horizontal transfers into the ancestor of spirochetes accompanied by displacement of the original gene. One well-studied case in this category is class I lysyl-tRNA synthetase, which apparently was acquired from the archaea (37, 78); similar evidence of archaeal origin was obtained for the two subunits of phenylalanyl-tRNA synthetase (78). By contrast, the synthetases for arginine, glutamate, methionine, isoleucine, and serine showed evidence of likely horizontal transfer from eukaryotic sources (78).