Lyme disease is caused by Borrelia burgdorferi, a bacterium transmitted to humans by ticks found in certain regions of the United States. Every year, around 300,000 people are diagnosed with Lyme disease, which can wreak havoc on the immune system. These patients often experience fevers, headaches, chronic fatigue, and skin conditions. Left untreated, Lyme disease can manifest as more serious abnormalities affecting the nervous system, cardiovascular system, and can even trigger other autoimmune conditions like arthritis.
New cases of Lyme disease are treated with antibiotics, with most patients making a positive recovery. However, some patients experience post-treatment Lyme disease syndrome – where symptoms can last for months. Post-treatment Lyme disease is difficult to treat, and doctors are unsure why only some patients experience this specific complication.
To better understand why some patients develop symptoms even after treatment of Lyme disease, researchers at John Hopkins studied the immune system at different stages of Lyme disease. By measuring inflammatory cells released by the liver during inflammation, they hoped to find a biological “signature” of early Lyme disease stages. The study included 44 patients with Lyme disease and 23 health participants for comparison. Researchers noticed that in the Lyme disease group, there were two subsets of early stages – those with high levels of inflammatory mediators, and those with lower levels. Patients who had a high expression of inflammatory mediators reported more severe symptoms, had higher rates of bacterial antibody production, higher rates of liver enzymes, and lower white blood cell counts. The elevated liver enzymes indicate infection, specifically in the liver.
The study suggests that levels of inflammatory mediators are indicative of symptom severity, and even disease outcomes. It’s likely that patients who have difficulty overcoming Lyme disease, even after treatment, have higher than average levels of inflammatory mediators circulating in their blood. Understanding the effects of prolonged inflammation after therapy could help researchers identify specific biomarkers that help to warn that a patient may experience post-treatment Lyme disease. Furthermore, finding drugs that block these specific biomarkers can prevent the onset of post-treatment Lyme disease by inhibiting inflammatory cell migration into blood and tissues.
This type of research can be somewhat difficult, as researchers note that Lyme disease is not a uniform condition, and can include a variety of symptoms and outcomes. However, one thing that all Lyme disease patients have in common is the involvement of immune pathways. These pathways are controlled by different elements in the immune system. Future studies will likely explore the elements of the immune system that control pathways involved in Lyme disease. It would be interesting to see if patients who have history of autoimmune conditions are more susceptible to post-treatment Lyme disease syndrome. By exploring these risk factors, healthcare professionals will one day be able to administer and prescribe specific anti-inflammatories tailored to each patient and the susceptibility of their immune dysfunction based on health history. Overall, the current evidence implicates that preventing excessive inflammation can have beneficial outcomes in Lyme disease, including the prevention of post-treatment Lyme disease syndrome.