Bartonella is a genetically diverse group of vector-borne bacteria. Over 40 species have been characterized to date, mainly from mammalian reservoirs and arthropod vectors. Rodent reservoirs harbor one of the largest Bartonella diversity described to date, and novel species and genetic variants are continuously identified from these hosts. Yet, it is still unknown if this significant genetic diversity stems from adaptation to different niches or from intrinsic high mutation rates. Here, we explored the vertical occurrence of spontaneous genomic alterations in 18 lines derived from two rodent-associated Bartonella elizabethae-like strains, evolved in non-selective agar plates under conditions mimicking their vector- and mammalian-associated temperatures, and the transmission cycles between them (i.e. 26 °C, 37 °C, and alterations between the two), using mutation accumulation experiments.
After ∼1000 generations, evolved genomes revealed few point mutations (average of one-point mutation per line), evidencing conserved single-nucleotide mutation rates. Interestingly, three large structural genomic changes (two large deletions and an inversion) were identified over all lines, associated with prophages and surface adhesin genes. Particularly, a prophage, deleted during constant propagation at 37 °C, was associated with an increased autonomous replication at 26 °C (the flea-associated temperature). Complementary molecular analyses of wild strains, isolated from desert rodents and their fleas, further supported the occurrence of structural genomic variations and prophage-associated deletions in nature. Our findings suggest that structural genomic changes represent an effective intrinsic mechanism to generate diversity in slow-growing bacteria and emphasize the role of prophages as promoters of diversity in nature.
Bacteriophages or simply phages were discovered in the early 1900’s and are viruses which infect a bacterium causing horizontal gene transfer which in turn causes bacterial evolution.
If you don’t know it yet, what goes into a Lyme/MSIDS patient is not what comes out. These critters morph inside us turning into something quite different, which is one reason this complex is so difficult to treat.
When I read a book on antibiotic resistance, thankfully something that is not occurring yet in Lyme/MSIDS with few exceptions, I learned of phage therapy. If this interests you check this out (located in the Republic of Georgia): https://www.phagetherapycenter.com/pii/PatientServlet?command=static_phagetherapy
News articles on phage therapy: https://www.phagetherapycenter.com/pii/PatientServlet?command=static_news&secnavpos=4&language=0
I’ve been told phage therapy wouldn’t work with Lyme/MSIDS due to the lack of host specificity. In other words, the phage must directly line up with the specific bacteria in order to work. Also, most of us are dealing with more than one bacteria, and battle worms, parasites, and other lovely beasts thrown into the mix to keep us humble.
The take home from this abstract is that the bacteria we are infected with are intelligent and stealthy, changing within us to further their goals. They don’t want to kill us, just maim and weaken us so they can live long, full lives. Also, notice “slow-growing bacteria,” which should serve as a clue to practitioners that these types of organisms scoff at 21 days of antibiotics.