By Fred Diamond
One of the most common questions I hear from Lyme survivors is simple but deeply loaded: “Why did this happen to me? Why did I get Lyme when others didn’t?”
If you’ve ever asked yourself, “Why me?” know that you’re not alone.
Thousands of Lyme survivors have pondered that same question. They were healthy. They were hiking. They were gardening. They were kayaking. They were simply living their lives. And then something changed.
On this week’s Love, Hope, Lyme podcast, Dr. Jennifer Miller of Galaxy Diagnostics, a scientist who has spent her career studying the Lyme bacterium, Borrelia burgdorferi, discusses why Lyme happens and why its effect may differ from person to person.
Her explanation reveals just how complex, and insidiously strategic, this organism truly is.
It starts in the wild
Lyme disease is what scientists call a vector-borne infection. In simple terms, that means it is transmitted by a vector and in this case, ticks.
But ticks are not born infected.
“The tick has to pick it up from a host that’s already infected,” Dr. Miller explains. “The larval tick will feed on an infected animal… and acquire the infection.”
That infected animal is usually a small mammal such as a mouse, chipmunk, or squirrel. These animals act as reservoir hosts. They carry the bacteria without becoming visibly sick.
After feeding, the tick molts into a nymph which is the stage most responsible for transmitting Lyme to humans. Nymphs are tiny, often no bigger than a poppy seed, and difficult to detect.
Many people assume deer are the main source of Lyme. Dr. Miller clarifies the nuance.
“Deer can have Lyme disease, but people aren’t going to get it from a deer.”
Deer play a role in the tick life cycle, but they are not the direct cause of human infection. The real issue is ecological.
“Because we have all these reservoir hosts, it’s a big part of the problem as to why Lyme disease incidence is increasing and why it’s spreading,” she says. “As humans, we occupy and consume more and more space… we’re encroaching on the territory of the deer, and with that, very unfortunately, comes Lyme disease.”
In other words, Lyme is not random. It is the byproduct of an expanding interface between humans and the natural infection cycle.
Borrelia is not an ordinary bacterium
Lyme disease is caused by a bacterium, not a virus, but it behaves unlike most bacteria.
Borrelia belongs to a family called spirochetes. It has a corkscrew shape that gives it unusual mobility.
“Borrelia will literally outrun the immune system,” Dr. Miller says. “Because it’s a corkscrew, it literally will burrow into the tissues.”
That corkscrew motion allows it to penetrate deeply into connective tissue, joints, and even cross protective barriers like the blood-brain barrier.
Even more concerning, Borrelia is highly adaptive.
“It literally will coat itself with host proteins. That allows it to evade immune detection.”
Camouflage
In essence, the bacterium can camouflage itself. It changes the proteins on its surface depending on whether it is inside a tick or inside a human. Once inside the body, it can alter its “coat” again to hide from immune surveillance.
Unlike some bacteria that cause disease by releasing toxins, Borrelia’s damage often comes indirectly.
“They’re not making toxins or poisons like other bacteria,” Dr. Miller explains. “But a lot of what happens with Borrelia is triggered by the immune system.”
The medical literature uses the phrase immune dysregulation to describe this phenomenon.
“Borrelia really interferes with the immune system,” she says.
In some individuals, the immune response becomes excessive and inflammatory, leading to joint damage, neurological symptoms, and widespread pain. In others, the immune response is blunted or misdirected, allowing the bacterium to persist quietly.
Why do some people get so sick while others don’t?
This may be the most painful question Lyme survivors ask.
“That’s still the biggest question that we need to answer,” Dr. Miller says candidly. “What I’ll tell you quite openly is that we don’t have all the answers.”
But there are clues.
Different strains of Borrelia produce slightly different surface proteins.
“Depending on which version of those proteins they’re making, some of those versions disagree with certain humans more than others.”
Some strains provoke a strong immune reaction. Others may slip past immune detection more easily.
Borrelia also actively interferes with antibody production.
“Borrelia will interfere with the timing of the antibody response. It interferes with the strength of the antibody response,” she explains. “It will trick them and confuse them so that they don’t produce antibodies in the right timeframe or of the right strength.”
This has enormous implications. If the immune system does not respond in a predictable way, both symptoms and laboratory tests become harder to interpret.
Host factors matter too. Genetics, previous infections such as Epstein-Barr virus, co-infections, mold exposure, chronic stress, and environmental burdens may all influence how a person responds.
There is likely no single reason why one person clears infection and another develops chronic symptoms. It is a complex interaction between pathogen and host.
The complication of co-infections
Lyme rarely travels alone.
“The number of different pathogens that were in the tick was far more than anybody would’ve thought… easily dozens,” Dr. Miller notes.
Ticks may carry Borrelia along with Babesia (a parasite similar in some ways to malaria), Bartonella (a different type of bacteria), Anaplasma, Ehrlichia, and even viral pathogens.
“You really have a lot of diversity of pathogens with these co-infections. That’s part of why they can be so very difficult to treat.”
A tick can acquire pathogens from one animal, survive the molt, then feed on another animal and acquire additional organisms. Birds, which can transport infected ticks across geographic regions, add another layer of complexity.
This microbial diversity means that two people bitten by ticks in different environments may experience very different symptom patterns.
Why testing fails so often
Few topics frustrate Lyme patients more than testing.
The standard two-tier antibody testing protocol has been in use for more than three decades. It measures antibodies but not the bacteria itself.
“The current tests are detecting that antibody response, and that can be very tricky,” Dr. Miller explains.
Antibodies only tell you that your immune system has seen the pathogen at some point. They do not reliably indicate active infection. And because Borrelia interferes with antibody production, some people never produce a strong enough response to meet diagnostic thresholds.
“Not everybody even generates an antibody response to Borrelia, one that’s strong enough or in line with what our out-of-date tests measure.”
False negatives can occur. Partial antibody bands may appear but not meet reporting criteria. Cross-reactivity with other infections can create additional confusion.
Adding to the challenge, Borrelia does not remain in high concentrations in the bloodstream.
“They don’t hide out at large numbers in the blood. There’s just not a lot of Borrelia in the blood.”
After transmission through the skin, the bacteria migrate into tissues. Blood-based detection becomes inherently difficult. This is why some researchers are working to develop direct detection methods, including antigen testing strategies.
“Borrelia are unique,” Dr. Miller explains. “When Borrelia shed their outer proteins it just gets released into the environment.”
Unlike many bacteria, Borrelia sheds structural components that may be detectable in other bodily fluids, offering a potential alternative to antibody-based testing.
A final word to patients
Lyme disease is biologically complex. It is ecologically driven. It is immunologically disruptive, and it does not behave like many other infections.
The science is still evolving. Researchers do not have all the answers.
But one thing is clear.
“If you think you have symptoms of Lyme disease and you haven’t seen a tick and you don’t have that bull’s-eye rash, please don’t assume that you don’t have Lyme disease,” Dr. Miller urges. “Go and get checked out.”
For survivors searching for understanding, the question why did this happen may never have a simple answer. But understanding biology, ticks, the bacterium, the immune system, and the co-infections can bring clarity.
And the more we understand that organism, the closer we move toward better diagnostics, better treatments, and better outcomes for every Lyme survivor.
Visit the Galaxy Diagnostics website to learn more about Lyme disease testing.
Click here to listen to all episodes of the Love, Hope, Lyme Podcast or on YouTube.
