Lyme Disease and Papilledema: A Retrospective Study on Clinical Characteristics and Outcomes.

Vesiculobullous Lyme disease: A case series

Diagnosis and Treatment of Lyme Disease

Lyme disease.

Lyme disease (LD) is the most commonly diagnosed tick-borne disease in North America and parts of Europe. Current mitigation strategies rely on personal protective behaviours, early diagnosis, and antibiotic treatment. This review updates on previous reviews on educational interventions for the prevention of LD and examines the impact of different interventions on the knowledge, attitudes and behaviours of healthcare professionals and the general public. We searched six databases for studies reporting participant assessment on knowledge, attitudes, and behaviours related to LD. We included studies targeting the public as well as healthcare professionals. We used keywords related to Lyme disease, health knowledge, attitudes, practices, community, health education, prevention, diagnosis, and treatment. Fourteen studies were included in this review; 13 reported educational interventions focused on the prevention of LD in the public, and one on physicians’ diagnosis of LD. Regardless of the type of intervention, the public’s knowledge (11/13 studies) were generally observed to improve post-intervention, though changes to preventive behaviours and attitudes were inconsistent. A key finding in this study was that no studies reported outcomes from interventions targeted at educating healthcare professionals on their knowledge of LD, or how to treat LD. Our review demonstrated that public health interventions enhance assessed and/or perceived LD knowledge. However, more research is needed to investigate interventions directed at healthcare professionals across the spectrum of LD: prevention, diagnosis, and treatment of early, late and post-treatment illness. PROSPERO 2019.

BackgroundThe nervous system is known to be the third most commonly (12–15%) affected site in Lyme disease (LD) in the U.S. Though previous studies reported peripheral neuropathy, encephalopathy, and encephalitis with some frequency in later stage LD, limited contemporary data exist on the frequency, presentation, and outcomes of these entities.MethodsRetrospective review of 1261 patients referred (2000–2013, single center) for presumptive LD was performed for neuroborreliosis. Symptoms less than 3 months were designated early LD. Patients with remote history of treated neuroborreliosis (> 2 years) were excluded. The diagnosis of LD followed CDC criteria. Response to antibiotics was assessed at the last clinical visit.ResultsOf 185 diagnosed with LD, 19% (35/185) had neuroborreliosis, including 29 early LD (ELD) and 6 late LD (LLD). The mean age was 44 yrs (±20) in ELD and 61(±11) in LLD. The median symptom duration was 14d (1–69) in ELD and 182d (140–2570) in LLD. Facial nerve palsy was most common, 54% (19/29 in ELD vs. 0/6 in LLD), followed by meningitis 20% (4/29 vs. 3/6), radiculopathy 20% (6/29 vs. 1/6), encephalopathy 3% (0/29 vs. 1/6), and peripheral neuropathy 3% (0/29 vs. 1/6) (P = 0.001). No encephalitis was identified. The median treatment duration (days) was 30 (10–135) in ELD and 56 (28–230) in LLD. All 35 patients were treated with doxycycline and/or ceftriaxone (16, 46% IV). Of the 32 followed patients, 28/32 (88%) responded to antibiotics, whereas 4/32 (12%) remained symptomatic with median follow-up duration of 72 days. Four non-responsive cases included 1 ELD (radiculopathy) and 3 LLDs (meningitis, encephalopathy, and peripheral neuropathy). The rate of non-response to antibiotics was higher in late LD (4% of ELD vs. 60% of LLD; P = 0.008). There was no statistically significant difference between outcome groups when comparing age, treatment duration, history of anxiety/depression, and route of treatment (p > 0.05, respectively).ConclusionEncephalopathy, encephalitis, and peripheral neuropathy ascribed to LD were uncommon in this population and poorly responsive to antibiotics. This raises the question whether LD truly was causal or if irreversible damage occurs by late stage LD. Future studies are needed in this regard.DisclosuresAll authors: No reported disclosures.

Editorial Commentary: Toward a Better Understanding of European Lyme Neuroborreliosis

BackgroundCasts are frequently used as routine treatment in paediatric orthopaedic practice, and yet are not without complications. At our large tertiary care paediatric hospital, baseline rate of all casting complications...

Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 Guidelines for the Prevention, Diagnosis, and Treatment of Lyme Disease.

Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 Guidelines for the Prevention, Diagnosis, and Treatment of Lyme Disease.

Lyme disease: authentic imitator or wishful imitation?

A Lyme disease (LD) diagnosis can be far from straightforward, particularly if erythema migrans does not develop or is not noticed. Extended courses of antibiotics for LD are not recommended, but their use is increasing. We sought to elucidate the patient patterns toward a diagnosis of LD, hypothesizing that a subset of patients ultimately receiving extended courses antibiotics may be symptomatic for an extended period before the first LD diagnosis. Claims submitted to a nationwide U.S. health insurance plan in 14 high-prevalence states were grouped into standardized diagnostic categories. The patterns of diagnostic categories over time were compared between patients evaluated for LD and given standard antibiotic therapy (PLDSA) and patients evaluated for LD and given extended antibiotic therapy (PLDEA) in 2011-2012. The incidence of PLDSA was 40.45 (N = 3207) and that of PLDEA was 7.57 (N = 600) per 100,000 insured over 2011-2012. 50.3% of PLDEA were diagnosed in the nonsummer months. Seven diagnostic categories were associated with PLDEA. From 180 days before the first LD diagnosis, the risks of having claims associated with back problems (odds ratio [OR], 2.1; confidence interval [95% CI], 1.4-2.9; p < 0.001) and connective tissue disease (OR, 1.6; 95% CI, 1.1-2.3; p < 0.01) complaints were higher among PLDEA. From 90 days before the diagnosis, malaise and fatigue (OR, 1.7; 95% CI, 1.1-2.6; p < 0.05), other nervous system disorders (OR, 2.0; 95% CI, 1.3-3.1; p < 0.01), and nontraumatic joint disorder (OR, 1.4; 95% CI, 1.0-2.0; p < 0.05) were more likely found among PLDEA than PLDSA. From 30 days before the diagnosis, the risk for mental health (OR 1.6; 95% CI, 1.1-2.0; p < 0.01) and headache (OR 1.5; 95% CI, 1.1-2.0; p < 0.05) among PLDEA was elevated. Among patients evaluated for LD and ultimately receiving an extended course of antibiotics for LD, 15.8% of them were symptomatic and seeking care for several months before their first LD diagnosis.

ALTHOUGH LYME DISEASE WAS FIRST RECOGNIZED 25 years ago, serologic methods of diagnosis have not been well standardized, and there is significant variability between laboratories. In the absence of a criterion standard blood test, the diagnosis of Lyme disease is based on a characteristic clinical picture in the appropriate epidemiologic setting (often supported by serologic data). Because the initial IgM response to the causative spirochete Borrelia burgdorferi characteristically begins 1 to 2 weeks after infection, patients with early classic Lyme disease may be antibody-negative. Conversely, B burgdorferi expresses crossreactive antigens and false-positive test results may occur, even using the recommended 2-step system of enzyme-linked immunosorbent assay (ELISA) screening (high sensitivity) followed by Western immunoblot (high specificity). To further complicate the issue, all the currently licensed ELISA tests contain the OspA surface antigen and, therefore, are invalid for individuals who have received the Lyme disease vaccine (composed of purified OspA). For patients with classic presentations of Lyme disease, there is widespread agreement about the initial diagnosis and antibiotic management. However, without a serologic criterion standard, there is no valid way to address issues of asymptomatic or atypical infection for long-term outcomes. The situation is analogous to the early years of the acquired immunodeficiency syndrome, when the case definition was entirely clinical and only patients with the most classic presentations (eg, Pneumocystis carinii pneumonia or Kaposi sarcoma) were considered to represent acquired immunodeficiency syndrome cases. With the advent of reliable human immunodeficiency virus testing in 1985, the case definition was broadened to include a variety of additional presentations (eg, recurrent Candida or Mycobacterium aviumintracellulare infection), and studies of the epidemiology and natural history of the infection quickly followed. Uncertainty breeds strong disparate opinions. As long as Lyme disease is defined primarily by its clinical characteristics, legitimate disagreement will exist between those who acceptonly thenarrowcasedefinition, limited to thosepatients with well recognized Lyme disease manifestations, and those who believe that B burgdorferi also may be an important contributor to other, less well-defined illnesses, particularly when accompanied by positive (albeit imperfect) serologic test results. Physicians who accept less stringent criteria argue that the full spectrum of Lyme disease is not known and that the strict diagnostic criteria may recognize only the tip of the iceberg.Concernabout inadequatelydiagnosedor treatedB burgdorferi infection is heightened by comparisons to syphilis, another disease caused by a spirochete, in which subtle, proteansignsandsymptomsmayprogress insidiously ifnot treated effectively. For the highly motivated patient seeking a diagnostic label for persistent symptoms, it is not difficult to find a physician who, reasoning that the response to a course of antibiotics represents a diagnostic trial, is willing to treat for the unlikely possibility of Lyme disease. This “doctor’s dilemma” is addressed in this issue of THE JOURNAL by Seltzer and colleagues in their assessment of long-term outcomes of patients who were diagnosed as having Lyme disease and reported to the Connecticut Department of Public Health from 1984 to 1991. Their random subsample of 8764 patients with reported Lyme disease netted 678 enrollable study patients, the largest group of patients with Lyme disease followed up in a longitudinal study. It is reassuring that after a median follow-up of 51 months, patients with a diagnosis of Lyme disease that met the national surveillance case definition developed by the Centers for Disease Control and Prevention (CDC) had the same profile of symptoms and the same quality-of-life indicators as age-matched controls without Lyme disease. Thus, recognition and treatment of clear-cut Lyme disease resulted in a return to baseline with no measurable sequelae. On the other hand, patients who were reported to have Lyme disease but who did not meet the CDC’s case definition of Lyme disease had increased symptoms and worsening quality-of-life indicators. The implication is that many of these individuals really did not have Lyme disease and therefore did not respond to the treatment. Although this study used accepted epidemiologic methods and analyses, it is surprising that only 64.3% of cases reported to the state met the current CDC national surveillance definition of Lyme disease. Moreover, not all patients

Phillip Baker has taken “Lyme denialism” to new depths (1). According to the Institute of Medicine, there are at least 116 million people living with acute and chronic pain in the United States. According to Baker, not one of those individuals suffers from chronic Lyme disease as a result of persistent infection with the Lyme spirochete, Borrelia burgdorferi. What is the basis for his opinion? Baker claims that “there is no evidence to indicate that chronic Lyme disease is due to a persistent infection” or that “extended antibiotic therapy is beneficial and safe”. This denialist statement about a disease that causes pain and suffering equivalent to that of diabetes or congestive heart failure ignores a growing body of evidence from the peer-reviewed medical literature that contradicts his opinion (2–5). Baker starts by attacking “Lyme-literate” physicians who use a “Lyme disease specialty laboratory” to diagnose tick-borne disease in a manner that is inconsistent with the surveillance case definition established by the Centers for Disease Control and Prevention (CDC). What Baker fails to tell us is that the CDC admits that its surveillance case definition “was developed for national reporting of Lyme disease” and was “not intended to be used in clinical diagnosis” (6). Thus, the diagnostic approach that Baker endorses is inappropriate for diagnosis of Lyme disease. Furthermore, the 46 patented commercial laboratory tests that Baker recommends for Lyme disease diagnosis have a sensitivity of only 46% and appear to yield results that are biased against women (7–9). Consequently, these commercial tests miss more than one-half of the patients with chronic Lyme disease in the United States. In contrast, the maligned “Lyme disease specialty laboratory” uses diagnostic criteria based on evidence from the peerreviewed medical literature (10, 11), and its “genderneutral” testing has a sensitivity and specificity of 90% (12). Clearly, this testing is preferable for the diagnosis of Lyme disease. As for Baker’s pat statement that “there is no evidence to indicate that chronic Lyme disease is due to a persistent infection,” numerous reports of veterinary cases and animal models confirm persistent infection with the Lyme spirochete in gerbils, hamsters, mice, dogs, monkeys, birds, and horses (13– 15). Among these cases, persistent pathology was seen in mice, dogs, and horses after the animals failed short-course treatment for their infection. Furthermore, there are at least 27 reports of persistent symptoms and failure to eradicate B. burgdorferi infection in humans treated with short-course antibiotic therapy for their tick-borne disease (5). Why does Baker deny these reports? He does so because they do not fit his limited view of Lyme disease. Baker also attacks the safety and efficacy of prolonged antibiotic therapy for chronic Lyme disease, stating that “all of the evidence obtained thus far...indicates no significant benefit as well as serious safety problems” with extended antibiotic therapy for these patients. What Baker fails to tell us is that the number of patients in controlled trials of Lyme disease treatment totals a mere 221 highly selected subjects who do not represent the vast majority of patients with chronic Lyme disease (3–5). Further analysis of these studies reveals that they were “of questionable quality”, lacked the power to detect potentially positive treatment effects, and failed to report predefined endpoints (16). Even so, in two of the four controlled trials, a significant benefit was seen in fatigue and cognition with the limited antibiotic regimen that was used, and safety problems were minimal (17, 18). In larger studies of extended antibiotic therapy, the safety of this treatment was shown to be acceptable, and the benefit of extended therapy was significant in terms of cognition, fatigue, and myalgic pain, although it took 6 –12 months of i.v. therapy to achieve this benefit (19, 20). In summary, Baker’s denialist view of the Lyme disease epidemic ignores significant evidence from the peer-reviewed medical literature that contradicts his opinion. It follows that practitioners who subscribe to his narrow view are abandoning the multitude of patients with acute and chronic pain who would benefit from treatment for their persistent spirochetal infection.

Electrocardiogram as a Lyme Disease Screening Test

Pediatric status epilepticus: How common is cerebrospinal fluid pleocytosis in the absence of infection?