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Borrelia burgdorferi is a bacterial species of the spirochete class of the genus Borrelia. B. burgdorferi exists in North America and Europe and until 2016 was the only known cause of Lyme disease in North America (Borrelia mayonii, found in the midwestern US, is also known to cause the disease).[1][2] Borrelia species are considered gram-negative.[3]
source:  Wikipedia

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Borrelia burgdorferi is a bacterial species of the spirochete class of the genus . B. burgdorferi exists in North America and Europe and until 2016 was the only known cause of Lyme disease in North America ( Borrelia mayonii, found in the midwestern US, is also known to cause the disease). Borrelia species are considered gram-negative.

Borrelia burgdorferi is named after the researcher Willy Burgdorfer, who first isolated the bacterium in 1982. Borrelia species is the species complex known to cause Lyme disease are collectively called Borrelia burgdorferi.

B. burgdorferi resembles other spirochetes in that it has an outer membrane and inner membrane with a thin layer of peptidoglycan in between. However, the outer membrane lacks lipopolysaccharide. Its shape is a flat wave. It is about 0.3 μm wide and 5 to 20 μm in length.

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.

B. burgdorferi is a slow-growing microaerophilic spirochete with a doubling time of 24 to 48 hours.

B. burgdorferi circulates between ticks and a vertebrate host in an enzootic cycle. B. burgdorferi living in a tick cannot be passed to its offspring. Therefore, tick larvae must feed on the blood of an infected animal to acquire B. burgdorferi, which ends up in the midgut. The spirochetes survive as the larvae molts into a nymph and persist in the nutrient-poor midgut as the nymph overwinters. Infected nymphs then transmit B. burgdorferi by feeding on another vertebrate to complete the cycle. Ticks can transmit B. burgdorferi to humans, but humans are dead-end hosts, unlikely to continue the life cycle of the spirochete. Nymphs molt into adult ticks, which usually feed on larger mammals that are not able to support the survival of B. burgdorferi.

Lyme disease is a zoonotic, vector-borne disease transmitted by the tick (also the vector for and ). The infected nymphal tick transmits B. burgdorferi via its saliva to the human during its blood meal.

Clinical presentation of Lyme disease is best known for the characteristic bull's-eye rash (also known as erythema chronicum migrans) but can also include myocarditis, cardiomyopathy, arrythmia, arthritis, arthralgia, meningitis, neuropathies, and facial nerve palsy depending on the stage of infection.

B. burgdorferi infections have been found in possible association with primary cutaneous B-cell lymphomas (PCBCLs), where a review of the primary literature has, as of 2010, noted that most of the PCBLCs examined have been 'unresponsive' to antibiotics; hence, as in the case of Chlamydophila psittaci association with ocular adnexal mucosa-associated lymphoid tissue (MALT) lymphoma, the working conclusion was that "if B. burgdorferi is truly associated with PCBCL, then there is wide geographic variability and other factors are probably involved".

Progression of the disease follows 3 stages.

Stage 1 is known as the Early Localized stage and occurs approximately 3 days - 1 month after inoculation. It affects the local area around the bite and is characterized by local swelling and / or a red "bull's-eye" rash (also known as erythema chronicum migrans) seen as an erythematous circle encircling a defined center that expands outward. It can get as large as 15 cm in diameter. 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.

Stage 2 is known as the Early Disseminated stage and occurs weeks - months after infection if left untreated. The bacteria spreads via the blood through the body to affect the organs. It often presents with general symptoms such as fever, chills, fatigue, and lymphadenopathy as well as the organ-specific symptoms. It can affect the causing myocarditis and arrythmias such as Atrioventricular blocks (which if significant enough may require the insertion of a pacemaker). It can affect the musculoskeletal system causing non-inflammatory transient arthritis and / or arthralgias. It can affect the nervous system manifesting as facial paralysis ( Bell's palsy, classically bilateral), fatigue, and loss of memory.

Stage 3 is known as the Late Disseminated stage and occurs months - years after the initial infection. Effects of the 3 rd stage include encephalitis or meningitis.. as well as migratory arthropathies (most commonly of the knee).

Anaplasmosis and babesiosis are also common tick-borne pathogens carried by the Ixodes tick that infect humans similarly to Borrelia burgdorferi. 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 Coinfected humans tend to display a more severe manifestation of Lyme disease. In addition, they tend to acquire a wider range of secondary symptoms, such as influenza-like symptoms. More studies and research must be done to determine the synergistic effect of co-infection and its effect on the human body.

So far, there are three factors that may contribute to the severity of the clinical manifestation of Lyme Disease. The presence of ribosomal spacers, plasmids, and the outer surface protein C (OspC) are indicators of the severity of the infection. Additionally, humans, themselves, vary in their response to the infection. The variation in response leads to different clinical manifestations and different infections to different organs.

This section needs expansion with: an encyclopedic description of the pathogenesis that is sourced to good secondary literature. You can help by adding to it.

After the pathogen is transmitted, it will acclimate to the mammalian conditions. Borrelia burgdorferi will change its glycoproteins and proteases on its plasma membrane to facilitate its dissemination throughout the blood. While infecting, B. burgdorferi will express proteins that will interact with endothelial cells, platelets, chondrocytes, and the extracellular matrix. This interaction inhibits proper function of the infected areas, leading to the pathological manifestations of Lyme disease. In response, the host will initiate an inflammatory response to attempt to remove the infection.

Borrelia burgdorferi, also, expresses at least seven plasminogen binding proteins for interference of factor H at the activation level. This is part of a complement system evasion strategy that leads to downstream blocking of immune response.

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.

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. Overall, B. burgdorferi's genome oddly consists of one megabase chromosome and a 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. Some of the plasmids are necessary for the B. burgdorferi life cycle but not for propagation of the bacteria in culture.

The genomic variations of B. burgdorferi contribute to varying degrees of infection and dissemination. 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. The OspC surface protein is shown to be a strong indicator of the identification of genomic classification and the degree of dissemination. Varying number of OspC loci are indications and determinants for the variations of B. burgdorferi. The surface protein is also on the forefront of current vaccine research for Lyme disease via Borrelia.

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.

In negative frequency-dependent selection, rare and uncommon variants will have a selective advantage over variants that are very common in an environment. For B. burgdorferi, low-frequency variants will be advantageous because potential hosts will be less likely to mount an immunological response to the variant-specific OspC outer protein.

Ecological niches are all of the variables in an environment, such as the resources, competitors, and responses, that contribute to the organism's fitness. Multiple-niche polymorphism states that diversity is maintained within a population due to the varying amount of possible niches and environments. Therefore, the more various niches the more likelihood of polymophrism and diversity. For B. burgdorferi, varying vertebrae niches, such deer and mice, can affect the overall balancing selection for variants.

Velázquez, Encarna, Peix, Álvaro & Gómez-Alonso, Alberto, 2011, "Microorganismos y cáncer: evidencias científicas y nuevas hipótesis", Cirugía Española, vol. 89, no. 3, pp. 136-144. ISSN 0009-739X; doi:10.1016/j.ciresp.2010.08.006; accessed 16 July 2015. English translation.

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Borrelia burgdorferi is a bacterial species of the spirochete class of the genus . B. burgdorferi exists in North America and Europe and until 2016 was the only known cause of Lyme disease in North America ( Borrelia mayonii, found in the midwestern US, is also known to cause the disease).

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Borrelia burgdorferi circulates between Ixodes ticks and a vertebrate host in an enzootic cycle. Tick larvae must feed on the blood of an infected animal to acquire Borrelia burgdorferi, which ends up in the midgut. The spirochetes survive as the larvae molts into a nymph and persist in the nutrient-poor midgut as the nymph overwinters. Infected nymphs then transmit Borrelia burgdorferi by feeding on another vertebrate to complete the cycle.Ticks can transmit Borrelia burgdorferi to humans, but humans are dead-end hosts, unlikely to continue the life cycle of the spirochete. Nymphs molt into adult ticks, which usually feed on larger mammals that are not able to support the survival of the pathogen.

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Lyme disease is caused by Borrelia burgdorferi and is the most common vector-borne disease in the United States. Each year, approximately 30,000 cases of Lyme disease are reported to CDC by state health departments and the District of Columbia. However, this number does not reflect every case of Lyme disease that is diagnosed in the United States every year.

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Centers for Disease Control and Prevention

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Seek medical attention if you observe any of these symptoms and have had a tick bite, live in an area known for Lyme disease, or have recently traveled to an area where Lyme disease occurs.

Untreated Lyme disease can produce a wide range of symptoms, depending on the stage of infection. These include fever, rash, facial paralysis, and arthritis.

The appearance of the erythema migrans rash can vary widely.

Fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes may occur in the absence of rash

Erythema migrans (EM) rash (see photos):

Occurs in approximately 70 to 80 percent of infected persons

Begins at the site of a tick bite after a delay of 3 to 30 days (average is about 7 days)

Expands gradually over several days reaching up to 12 inches or more (30 cm) across

May feel warm to the touch but is rarely itchy or painful

Sometimes clears as it enlarges, resulting in a target or "bull's-eye" appearance

May appear on any area of the body

Does not always appear as a "classic" erythema migrans rash

Severe headaches and neck stiffness

Additional EM rashes on other areas of the body

Facial palsy (loss of muscle tone or droop on one or both sides of the face)

Arthritis with severe joint pain and swelling, particularly the knees and other large joints.

Intermittent pain in tendons, muscles, joints, and bones

Heart palpitations or an irregular heart beat (Lyme carditis)

Episodes of dizziness or shortness of breath

Inflammation of the brain and spinal cord

Nerve pain

Shooting pains, numbness, or tingling in the hands or feet

Page last reviewed:

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lyme disease (borrelia burgdorferi infection)

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Signs and symptoms of Lyme disease | CDC

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Seek medical attention if you observe any of these symptoms and have had a tick bite, live in an area known for Lyme disease, or have recently traveled to an area where Lyme disease occurs. Untreated Lyme disease can produce a wide range of symptoms, depending on the stage of infection.

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Fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes may occur in the absence of rash

Erythema migrans (EM) rash (see photos):

Occurs in approximately 70 to 80 percent of infected persons

Begins at the site of a tick bite after a delay of 3 to 30 days (average is about 7 days)

Expands gradually over several days reaching up to 12 inches or more (30 cm) across

May feel warm to the touch but is rarely itchy or painful

Sometimes clears as it enlarges, resulting in a target or “bull’s-eye” appearance

May appear on any area of the body

Does not always appear as a “classic” erythema migrans rash

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Lyme disease is diagnosed based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks.

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People treated with appropriate antibiotics in the early stages of Lyme disease usually recover rapidly and completely. Antibiotics commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axetil.

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The National Institutes of Health (NIH) has funded several studies on the treatment of Lyme disease that show most people recover when treated within a few weeks of antibiotics taken by mouth.

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Funding to further study and ultimately treat Lyme Disease

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Funding to further study and ultimately treat Lyme Disease

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Doctors can diagnose the disease through physical findings such as a "bull's-eye" rash along with a history of symptoms. But not everyone has the rash, and not everyone can recall being bitten. Special blood tests can be taken three to four weeks after suspected contact to confirm the diagnosis.

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Enzyme-linked immunosorbent assay (ELISA) test.

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Enzyme-linked immunosorbent assay (ELISA) test.

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The test used most often to detect Lyme disease is the ELISA and it detects antibodies to B. burgdorferi.

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Lyme disease can affect people of any age. People who spend time outdoors in activities such as camping, hiking, golfing, or working or playing in grassy and wooded environments are at increased risk of exposure. The chances of being bitten by a deer tick are greater during times of the year when ticks are most active.

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Deer ticks live in shady, moist areas at ground level. They will cling to tall grass, brush and shrubs, usually no more than 18-24 inches off the ground. They also live in lawns and gardens, especially at the edges of woods and around old stone walls.

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The Lyme disease bacterium, Borrelia burgdorferi, is spread through the bite of infected ticks. The blacklegged tick (or deer tick, Ixodes scapularis) spreads the disease in the northeastern, mid-Atlantic, and north-central United States.

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You can decrease your risk of getting Lyme disease by taking some simple precautions:
1. Cover up
2. Use insect repellents
3. Do your best to tick-proof your yard
4. Check your clothing, yourself, your children and your pets for ticks
5. Don't assume you're immune
6. Remove a tick as soon as possible with tweezers.