Borrelia (Borreliella) burgdorferi is a bacterial species of the spirochete class in the genus Borrelia, and is one of the causative agents of Lyme disease in humans. Along with a few similar genospecies, some of which also cause Lyme disease, it makes up the species complex of Borrelia burgdorferi sensu lato. The complex currently comprises 20 accepted and 3 proposed genospecies.
Microbiology
Borrelia burgdorferi is named after the researcher Willy Burgdorfer, who first isolated the bacterium in 1982.
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B. burgdorferi is a microaerobic, motile spirochete with seven to 11 bundled perisplasmic flagella set at each end that allow the bacterium to move in low- and high-viscosity media alike, which is related to its high virulence factor.
Metabolism
B. burgdorferi is a slow-growing microaerophilic spirochete with a doubling time of 24 to 48 hours.
Transformation
Bacterial transformation has been utilized by researchers in order to isolate specific pathogenic genes among the Borrelia burgdorferi. B. burgdorferi strains appear to be highly insufficient for use in bacterial transformation due to the large amount of DNA needed for transformation, the time it takes to produce reliable transformants, and the influence of restriction modification systems. In fact, infectivity of B. burgdorferi often requires the gene pncA, which is present on a bacterial plasmid that contains the gene bbe02 that is highly selected against during transformation. Since these genes are often paired together, infectivity is selected against in transformation, counteracting research to pinpoint particular genes that function in pathogenicity of Borrelia burgdorferi. Despite this, some headway has been made in unraveling the mysteries of B. burgdorferi, such as the discovery of gene cyaB as essential for mammalian infection.
Life cycle
B. burgdorferi circulates between Ixodes ticks and a vertebrate host in an enzootic cycle. rare cases of transovarial transmission have been reported, but may be attributable to Borrelia miyamotoi, a related spirochete. Once a tick is infected, it will then transmit B. burgdorferi by feeding on another vertebrate to complete the cycle. Nymphs molt into adult ticks, which usually feed on larger mammals that are not able to support the survival of B. burgdorferi.
Disease
B. burgdorferi is the causative agent of Lyme disease and is why this bacteria is so important and being studied. It is most commonly transmitted from ticks to humans. Humans act as the tick's host for this bacteria. Lyme disease is a zoonotic, vector-borne disease transmitted by the Ixodes tick (also the vector for Babesia and Anaplasma). The infected nymphal tick transmits B. burgdorferi via its saliva to the human during its blood meal. depending on the stage of infection. right|thumb|Characteristic "bull's-eye" (erythema chronicum migrans) rash of stage 1 Lyme disease
B. burgdorferi infections have been found in possible association with primary cutaneous diffuse large B-cell lymphomas (PCDLBCLs), where a review of the primary literature has, as of 2010, noted that most of the PCBCLs examined have been 'unresponsive' to antibiotics; Once the rash starts to subside the first symptoms can manifest as "flu-like" symptoms. At this stage, antibiotics are most efficacious to prevent further growth and symptoms of the disease before the major symptoms manifest. Consequently, it is possible for an Ixodes tick to coinfect a host with either two or all other diseases. When a host is coinfected, the combined effects of the diseases act synergistically, often proving to cause worse symptoms than a single infection alone While infecting, B. burgdorferi will express proteins that will interact with endothelial cells, platelets, chondrocytes, and the extracellular matrix.
In addition, Borrelia burgdorferi has a strategy to directly inhibit the classical pathway of complement system. A borrelial lipoprotein BBK32, expressed on the surface of Borrelia burgdorferi, binds the initiating protease complex C1 of the classical pathway. More specifically, BBK32 interacts with C1r subunit of C1. C-terminal domain of the BBK32 protein mediates the binding. As a result, C1 is trapped in an inactive form.
Genome
B. burgdorferi (B31 strain) was the third microbial genome ever sequenced, following the sequencing of both Haemophilus influenzae and Mycoplasma genitalium in 1995. Its linear chromosome contains 910,725 base pairs and 853 genes. The sequencing method used was whole genome shotgun. The sequencing project, published in Nature in 1997 and Molecular Microbiology in 2000, was conducted at The Institute for Genomic Research. B. burgdorferi genome consists of one megabase chromosome and an unusual variety of circular and linear plasmids ranging in size from 9 to 62 kilobases. The megabase chromosome, unlike many other eubacteria, has no relation to either the bacteria's virulence or to the host-parasite interaction. Each genomic group has varying antigens on its membrane receptor, which are specific to the infection of the host. One such membrane receptor is the surface protein OspC.
Bacteriophage
Relatively few bacteriophages are known to infect B. burgdorferi. Several phage particles were isolated and some evidence suggested that they had an 8-kb dsDNA genome. Among the best-studied Borrelia phages is φBB-1, a phage with a polyhedral head and a contractile tail of 90 nm in length. φBB-1 was the first bacteriophage that provided evidence of transduction for lateral gene transfer in Borrelia species that cause Lyme Disease. Current research aims to use bacteriophages as way of identifying virulence factors in spirochetes that lead to Lyme Disease.
Immune Response
Mounting a successful immune response to Lyme disease can be complex considering the amount of cells involved. There are two different aspects to the immune system that allow for rapid and long-lasting responses. The innate immune system allows for a rapid, non-specific response to a pathogen. While the adaptive immunes system allows for a more long-lasting response that is more specific. The macrophage is part of the innate immunity as it attempts to locate, bind, and phagocytose the bacteria into an endosome. This allows for killing of the pathogen. Cytokine release during this also helps to attack the bacteria. T-cells are part of the adaptive immunity. They are more specific and can differentiate into different types that all serve different roles. The ultimate goal of the T-cells is to produce cytokines that will recruit other immune cells to the infection to help fight it. Borrelia burgdorferi has the ability to avoid detection from host immune systems, which makes it difficult to attack the infection right when it starts. The bacteria utilizes the outer surface proteins and it able to switch between them, which makes detection rather difficult [43]. This is just one example of how this bacteria can invade the immune system and not be detected. The body response to this includes integration between the innate and adaptive immunity which, like previously mentioned, includes many players.
Evolution
Genetically diverse B. burgdorferi strains, as defined by the sequence of ospC, are maintained within the Northeastern United States. Balancing selection may act upon ospC or a nearby sequence to maintain the genetic variety of B. burgdorferi. Balancing selection is the process by which multiple versions of a gene are kept within the gene pool at unexpectedly high frequencies. Two major models that control the selection balance of B.burgdorferi is negative frequency-dependent selection and multiple-niche polymorphism. These models may explain how B. burgdorferi have diversified, and how selection may have affected the distribution of the B. burgdorferi variants, or the variation of specific traits of the species, in certain environments.
Negative-frequency dependent selection
In negative frequency-dependent selection, rare and uncommon variants will have a selective advantage over variants that are very common in an environment.
External links
- NCBI Borrelia Taxonomy Browser
- Borrelia burgdoferi B31 Genome Page
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