A fictional story …
Diffuse complaints …
Since weeks Lisa M. (36) feels exhausted, has aching legs and arms and has developed a fever. Initially, of course, she thought she had the flu. After a while she felt better. But now, the pain has come back: She has burning pain in her muscles and joints, especially at night, she has a terrible headache and sometimes even visual defects. She feels dizzy and her legs are numb, similarly to the left side of her face (facial nerve paresis). Since this morning, the corner of her mouth is hanging as if she has had an anaesthesie at the dentist.
It is time to visit the GP. Her symptoms are rather diffuse and unspecific and the GP has to perform some tests before he can establish a diagnosis. But he has a suspicion.
… Suspicion: acute Lyme neuroborreliosis …
Lyme neuroborreliosis is a severe form of tick-borne Lyme borreliosis (Lyme disease). This is caused by a bacterium called Borrelia burgdorferi which is transmitted to humans by a tick bite. In many cases of Lyme disease, a circular reddening (Erythema migrans) is the first symptom of Borrelia infection. It initially arises around the tick bite, expands in growing circles and may spread over the body (stage I).
Indeed, Lisa remembers a tick bite on the inner side of her left thigh, but this was already months ago. Definitely, there was no reddening around the bite. If she had observed any skin irritation, she would have gone to her GP directly.
Something that Lisa M. did not know: only in about half of all Lyme neuroborreliosis cases, does the reddening actually arise. After the tick bite, the Borrelia may spread in the body without being noticed and attack the central and peripheral nervous system (stage II) – that is why it is called neuroborreliosis. Symptoms may be inflammation of the meninges, nerves and nerve roots or even the brain, which causes pain and paralysis. The fast diagnosis of neuroborreliosis is crucial for an appropriate treatment of the patient.
… and a safe diagnosis
An acute Lyme neuroborreliosis is diagnosed only when further signs of the Borrelia infection can be detected in addition to the neurological complications. These include the detection of anti-borrelia antibodies in the cerebrospinal fluid (CSF) of the patient. The antibodies are produced by the immune system as defence against the Borrelia.
This antibody production, however, takes 7-10 days which is why sometimes anti-Borrelia antibodies cannot be detected in CSF particularly in early stages of infection. This may lead to a delayed diagnosis of Lyme neuroborreliosis. A signalling molecule of the immune system – CXCL13 – now may support rapid diagnosis of infection. Scientists discovered that the CXCL13 concentration in CSF is increased in Lyme neuroborreliosis patients even in early stages of disease, when anti-Borrelia antibodies are not yet produced. Therefore, CXCL13 is a promising novel biomarker to recognize acute Lyme neuroborreliosis early on.
The GP’s suspicion is confirmed when he receives the test results for his patient Lisa M.: antibodies against Borrelia are present in CSF and the tested CXCL13 concentration is considerably elevated. Lisa will be treated with antibiotics during the coming weeks. CXCL13 may also support therapy monitoring: if the CXCL13 level rapidly decreases, this is an indication of successful treatment and the decline of infection.