Lyme disease is caused by a bacterium, specifically a type called a spirochete. The pathogen responsible is Borrelia burgdorferi, a corkscrew-shaped microorganism that belongs to a family of bacteria known for their unusual structure and movement. It is not a virus, fungus, or parasite, though it does depend on ticks to spread from one host to another.
A Spirochete, Not a Typical Bacterium
Spirochetes are a distinctive group of bacteria defined by their long, coiled shape and unique way of moving. Borrelia burgdorferi has a flat, wave-like appearance with an undulating body that lets it bore through thick tissues like skin, cartilage, and joint fluid. This shape is central to what makes it effective as a pathogen.
What drives this movement is a bundle of 7 to 11 internal flagella (tiny whip-like structures) anchored at each end of the cell. Unlike most bacteria, whose flagella spin on the outside, these flagella are tucked between the cell’s inner and outer membranes, in a space called the periplasm. They rotate like a corkscrew drill, propelling the bacterium forward through environments that would stop most other microbes. Without these internal flagella, the organism loses both its characteristic shape and its ability to cause infection.
An Unusual Cell Structure
Under a microscope, B. burgdorferi resembles a Gram-negative bacterium in that it has both an outer membrane and an inner membrane surrounding its core. But the resemblance mostly ends there. Its outer membrane lacks a key sugar-based molecule found on virtually all other Gram-negative bacteria. Instead, the surface is studded with lipoproteins, fat-anchored proteins that play critical roles in how the organism interacts with ticks, animal hosts, and the human immune system.
This atypical surface is one reason Lyme disease can be tricky to diagnose and treat. The bacterium doesn’t trigger the same immediate immune alarm bells that more conventional bacteria do.
More Than One Species Causes Lyme
Borrelia burgdorferi is actually part of a larger family called the B. burgdorferi sensu lato complex, which contains more than 23 related species (called genospecies). Five of these are known to cause Lyme disease in humans: B. burgdorferi sensu stricto, B. afzelii, B. garinii, B. bavariensis, and B. spielmanii.
In North America, B. burgdorferi sensu stricto is the only species that causes Lyme disease. In Europe and Asia, the picture is more varied. B. afzelii tends to cause persistent skin symptoms, while B. garinii is more commonly associated with neurological complications. This species diversity is one reason Lyme disease can look different depending on where in the world someone is infected.
How It Spreads Through Ticks
The bacterium lives in a cycle between ticks and animal hosts, primarily small mammals like white-footed mice. In North America, blacklegged ticks (Ixodes scapularis in the eastern U.S. and Ixodes pacificus on the West Coast) are the vectors. These ticks go through a two- to three-year life cycle with four stages: egg, larva, nymph, and adult. They need a blood meal at every stage after hatching and pick up a new host each time.
Ticks typically acquire the bacterium during their larval or nymphal stages, when they feed on infected animals. They then pass it along to humans or other hosts during later feedings. In most cases, a tick must be attached for more than 24 hours before the bacterium can be transmitted. That delay happens because the spirochetes live in the tick’s gut and need time to migrate to the salivary glands before entering the host’s skin.
How It Survives in the Human Body
Once inside a person, B. burgdorferi has several biological tricks that help it persist. One of the most important is antigenic variation, a process where the bacterium continuously reshuffles a key surface protein called VlsE. The gene encoding this protein can swap segments with 15 silent backup copies stored elsewhere in the bacterium’s DNA, generating an enormous number of surface variations. Each time the immune system learns to recognize one version of VlsE, the bacterium has already switched to a new one. VlsE may also act as a physical shield, blocking antibodies from reaching other proteins on the cell surface.
The pathogen also has an unusual relationship with metals. Most disease-causing bacteria need iron to survive, but B. burgdorferi does not accumulate iron at all. This is significant because the human immune system often fights infection by restricting iron availability. By relying on manganese instead of iron for its essential enzymes and antioxidant defenses, the spirochete sidesteps this entire strategy. The lack of iron also means the bacterium avoids a common source of internal damage: iron-driven chemical reactions that generate toxic oxygen molecules inside bacterial cells.
How Infection Is Confirmed
Because the spirochete is difficult to grow in a lab and doesn’t circulate in the blood in large numbers, Lyme disease is diagnosed through antibody testing rather than by detecting the bacterium directly. The CDC recommends a two-step process using the same blood sample. The first test screens for antibodies against B. burgdorferi. If that result is positive or borderline, a second, more specific test is run to confirm. Both steps must be positive for the result to count.
The standard approach pairs an initial screening test with a more detailed test called a Western blot. An increasingly common alternative uses two screening-type tests in sequence, which can be faster and easier to standardize across laboratories. One important caveat: antibodies take time to develop, so testing in the first few days of illness can produce false negatives. A positive result on the early-stage antibody test is also considered unreliable if symptoms have been present for more than 30 days, since that type of antibody should have faded by then.