Lyme disease is caused by bacterium within the Borrelia burgdorferi speciescomplex, including B. burgdorferi sensu lato, B. burgdorferi sensu stricto, and B. mayonii.
In humans, the spirochetesare transmitted by the bite of an infected blacklegged tick. Lyme disease hasan incidence of roughly 300,000 cases a year, and it is the most common vectorborne disease in the United States. Lyme disease is primarily a diagnosed clinically,and laboratory testing is often used forconfirmation supporting the diagnosis. The hallmark of Lyme disease is erythema migrans, alsoreferred to as a bulls eye rash.
This rash is typically followed by flu likesymptoms, arthralgia, myalgia, headache, and fatigue, but not all cases will presentwith a rash. The signs and symptoms mentioned are commonly associated with thisdisease process. For Lyme disease, treatment with a short course of antibioticsof 10-28 days, is current practice. However, after treatment some patients willexperience symptoms similar to those experienced during the active infection. Is the standard treatment protocol enough to resolvethe infection of Lyme disease? Aresymptoms of post-treatment Lyme diseasesyndrome (PTLDS) related to bacteria that were not eradicated? Does standard pharmacologictherapy address all potential forms of the bacterium possibly present? Review of Literature: Inthe scientific community there is not a widely accepted standard definition ofpost -treatment Lyme disease syndrome, the lack of data on its pathogenesis hascaused confusion and controversy on the syndrome. The most widely accepteddefinition of Post-treatment Lyme disease syndrome describes the pattern of persistentsymptoms that continue for six months or greater after the completion oftreatment for Lyme disease. It has been reported that as many as 40-50% ofpeople treated early for the disease experience recurrent symptoms such as:chronic fatigue, cognitive dysfunction, myalgias, neuropathy, and joint pain.
Lyme disease causing bacteria have been noted to utilizemultiple forms of evasion, includingcyst formation, production of biofilms, spirochete form, and employing a tacticof intracellular evasion. Adding further complexity to the situation, Borreliais known to have the ability to change and manipulate outer surface proteinsregularly, this allows for immune cell evasion from the host. One study demonstrated that in monkeys there was persistence of bacteria in the heart; however, PCR, skinbiopsy cultures, and in vivo cultures were negative on analysis. Furtherfindings demonstrated that intact spirochetes were found in three out of fivetreated monkeys by xenodiagnosis at 12 months after the tick bite. Immuneresponses to B. burgdorferi were shown to vary significantly aftertreatment for Lyme disease.
Widespread variable microscopic disease, primarilyinflammation, was observed in all infected subjects, despite having receivedantibiotic treatment. Another area that makes this syndrome problematic happensto be that there is no definitive testing to verify curative therapy. On the other hand,diagnosing a reinfection without the characteristicerythema migrans is difficult, relying cautiously on acute serology forinsight. The question can be raised was the patient ever cured in the firstplace, or was the infection only subdued to an asymptomatic level? The sequelaexperienced from PTLDS could be hypothesized to be that the infection with theLyme causing bacterium was never eradicated in its entirety and is still causing the symptomatic condition to persist. Expected Outcomes: The goal of this literary study is to utilizecurrent research to hypothesize thepathogenesis of post treatment Lyme disease.
Explore the possible mechanisms ofevasion by the Borrelia species andaddress potential pitfalls in current therapeutic practices.