Symptoms Of Lyme Disease Research Articles

Cerebrospinal Fluid-Infiltrating CD4+T Cells RecognizeBorrelia burgdorferiLysine-Enriched Protein Domains and Central Nervous System Autoantigens in Early Lyme Encephalitis

Neurological manifestations of Lyme disease are usually accompanied by inflammatory changes in the cerebrospinal fluid (CSF) and the recruitment of activated T cells into the CSF compartment. In order to characterize the phenotype and identify target antigens of CSF-infiltrating T cells in early neuroborreliosis with central nervous system (CNS) involvement, we combined T-cell cloning, functional testing of T-cell responses with positional scanning synthetic combinatorial peptide libraries, and biometric data analysis. We demonstrate that CD4+ gamma interferon-producing T cells specifically responding to Borrelia burgdorferi lysate were present in the CSF of a patient with acute Lyme encephalitis. Some T-cell clones recognized previously uncharacterized B. burgdorferi epitopes which show a specific enrichment for lysine, such as the heat shock-induced chaperone HSP90. Degenerate T-cell recognition that included T-cell responses to borrelia-specific and CNS-specific autoantigens derived from the myelin protein 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) could be demonstrated for one representative clone. Our results show that spirochetal antigen-specific and Th1-polarized CD4+ lymphocytes infiltrate the CSF during monophasic CNS symptoms of Lyme disease and demonstrate that cross-recognition of CNS antigens by B. burgdorferi-specific T cells is not restricted to chronic and treatment-resistant manifestations.

Lyme myositis

Myositis has been reported as a rare manifestation of Lyme disease, and Lyme myositis can be an important consideration in the differential diagnosis of unusual cases, especially in patients who live in or travel to endemic areas. We report the case of a 43-year-old man who presented with focal myositis of the proximal lower extremity and was subsequently diagnosed as having Lyme myositis. The patient had previously experienced a febrile illness and rash, but had no ongoing symptoms of Lyme disease. Myositis was confirmed by magnetic resonance imaging and muscle biopsy; Borrelia burgdorferi infection was confirmed by Lyme serology and polymerase chain reaction testing of synovial fluid and biopsy material. The current case is reviewed in the context of findings from previous case descriptions.

Borrelia burgdorferiinIxodes scapularisTicks, Chicago Area

To the Editor: Lyme disease is a multisystem disorder associated with skin, myocardial, musculoskeletal, and central and peripheral nervous system manifestations caused by infection with Borrelia burgdorferi sensu lato spirochetes (1). In the United States, the illness is caused by transmission of B. burgdorferi sensu stricto from the bite of infected Ixodes scapularis (deer) ticks found primarily in the northeastern and upper midwestern United States (2). B. burgdorferi–infected ticks have also been recovered in portions of northern Illinois but have not yet been reported in the Chicago region (3). In fact, a previous survey (4) of forested areas in the heavily populated regions immediately adjacent to Chicago confirmed a low risk of contracting Lyme disease. Researchers failed to recover deer ticks from 7 sampling sites and recovered only a single Borrelia isolate from well-described B. burgdorferi sensu stricto rodent reservoirs (mice, voles, chipmunks) captured from 5 sampling sites. A subsequent genetic analysis confirmed the isolate was B. bissettii (5), a genomic group that is likely nonpathogenic to humans in the United States. However, the area of the Midwest where Lyme disease is endemic has continued to expand from its origin in northeastern Minnesota and northwestern Wisconsin (2,6). The Chicago metropolitan region has numerous parks and natural areas that are biologically similar to the known midwestern focus (7), and these areas support a large population of white-tailed deer. Moreover, we have seen anecdotal reports of persons with clinical signs and symptoms of Lyme disease and epidemiologic evidence that suggests local acquisition. Two ticks submitted by a resident who had hiked in DuPage County near the east branch of the DuPage River were I. scapularis. We therefore began searching for questing ticks in this area and 9 other geographically diverse areas of DuPage County. The 10 sites were flagged by dragging white cotton sheets through the underbrush for 2- to 10-hour intervals during the spring of 2005. We timed these collections on the basis of information that adult deer ticks were questing in Wisconsin. Recovered ticks were placed in sealed vials and transported to the North Park University Laboratory where their identity was confirmed. The midguts were then removed aseptically, and each was placed into a separate vial that contained 2 mL modified Barbour-Stoenner-Kelly medium that could support the growth of small numbers of B. burgdorferi sensu stricto (8). Cultures were incubated for 6 weeks at 35°C and examined weekly for spirochetes by darkfield microscopy. Deer ticks were not found at 8 of the DuPage County sample sites. However, 90 adult or nymphal I. scapularis were collected from the remaining 2 sites, and spirochetes were recovered from 3 (3%) of the tick midgut cultures. Because of these findings and anecdotal reports of deer ticks in Cook County, we also surveyed 3 sites in Cook County during the fall of 2005. Deer ticks were not found at 2 sites, but 37 adult I. scapularis ticks were collected from a site in the southwestern portion of Cook County, and spirochetes were recovered from 2 (5%) cultures. We first examined the protein profiles to identify the spirochetes. Sodium dodecyl sulfate–polyacrylamide gel electrophoresis analyses of 4 of the 5 isolates (1 isolate lost viability before analysis) showed that they were distinctly different from the B. bissettii isolate recovered previously from Cook County (4), but the isolates were strikingly similar to B. burgdorferi sensu stricto (Figure). We then amplified an intergenic spacer region of the rrf-rrl portion of the rRNA from 2 isolates by a previously described method (9) and sequenced the amplified products (sequencing by Laragen, Inc., Los Angeles, CA, USA). The sequences were identical to that of B. burgdorferi sensu stricto isolate B-31 (9). Figure Protein profiles of Borrelia burgdorferi sensu stricto (lane A), B. bissettii (lane B), and spirochetes from Ixodes scapularis ticks collected from DuPage County (lanes C, D) or Cook County (lanes E, F), Illinois. The results confirmed that I. scapularis ticks infected with B. burgdorferi sensu stricto were recovered from forested areas surrounding Chicago. Additional studies to define the extent and severity of the risk are necessary, but clinicians and the public should be aware of the possibility of acquiring Lyme disease in the Chicago metropolitan region.

Audit of the laboratory diagnosis of Lyme disease in Scotland

An audit was performed on the laboratory diagnosis of lyme disease in Scotland. The problem of a significant number of patients with clinical symptoms of lyme disease being reported as seronegative or equivocal by the confirmatory Western blot test was identified. Comparisons of current practice were made with American and European standards, and the Western blot scoring system revised. When applied retrospectively (April 2003 to March 2004), 39 (33 %) of 116 serum samples previously negative or equivocal became weak positive or stronger. Thirty-one (80 %) of these 39 samples were from patients with clinical details suggestive of early lyme disease. The changes were implemented and assessed prospectively for 6 months. There was a significant increase in the proportion of equivocal results, with fewer negatives compared to the same time period 1 year previously. This audit has helped clinicians in the diagnosis of lyme disease and the management of these patients in Scotland.

A comparison of two treatment regimens of ceftriaxone in late Lyme disease

The optimal duration of treatment for patients with late Lyme disease is unresolved. In a prospective, open label, randomized, multi-center study, a 14 day course of ceftriaxone was compared to 28 days of therapy. Entry criteria included objective abnormalities compatible with late Lyme disease and serologic reactivity to Borrelia burgdorferi. Randomization took place prior to obtaining serologic results. Clinical response was rated as cure; improvement; failure; or not assessable. Of the 201 patients randomized, 21 patients in the 14 day group and 37 in the 28-day group were excluded from the study for failure to meet serologic criteria. Of those who met serologic criteria, 80 patients received 14 days and 63 received 28 days of ceftriaxone. At time of last evaluation, there were 5 treatment failures in the 14 day group and none in the 28 day group (p = 0.07). Clinical cure rates were 76% for the 14 day group and 70% for the 28 day group (p = NS). Therapy was discontinued due to adverse events for a significantly greater proportion of patients in the 28-day group compared to the 14-day group (p < 0.02). Ceftriaxone for 14 days eradicated the signs and symptoms of late Lyme disease in the majority of evaluable patients. Although there were more failures in the 14-day group than in the 28-day group, this study did not have the power to determine if a clinical subset of patients may benefit from 28 days of therapy.

Improving the specificity of 16S rDNA-based polymerase chain reaction for detecting Borrelia burgdorferi sensu lato-causative agents of human Lyme disease

16S rDNA sequences of Borrelia burgdorferi sensu lato were aligned with the 16S rDNA sequences of Borrelia hermsii, Borrelia turicatae, and Borrelia lonestari in order to identify primers that might be used to more specifically identify agents of human Lyme disease in ticks in human skin samples. Standard polymerase chain reaction (PCR), using an oligonucleotide sequence, designated TEC1, was shown, in combination with a previously developed primer (LD2) to amplify strains of B. burgdorferi sensu stricto, Borrelia afzelii, and Borrelia garinii, but not the non-Lyme causing B. hermsii or B. turicatae. This primer pair, designated Bbsl, was successfully used to amplify B. burgdorferi sensu lato from skin biopsies of patients with Lyme disease symptoms as well as from Ixodes scapularis, Amblyomma americanum and Dermacentor variabilis ticks. The primer set Bbsl allows for the rapid detection and differentiation of B. burgdorferi sensu lato from non-Lyme disease-causing Borrelia species in ticks and human tissues. The PCR primer set, Bbsl, will greatly facilitate detection of the causative agents of Lyme disease in infected ticks and human skin samples assisting in epidemiological studies, and potentially allowing for a more rapid diagnosis of the disease in patients.

Is Gulf War Syndrome actually chronic Lyme disease?

Symptoms of Gulf War Syndrome and chronic Lyme disease are very similar. Lyme disease is a condition which can be difficult to diagnose since one of the main features of the condition, the erythema migrans rash, may be absent or overlooked and serological testing for Lyme disease may be falsely negative. Symptoms of Lyme disease may not became apparent until years after exposure to the causative organism. Military personnel during training in the field are at risk of tick bites and it may be that those who developed Gulf War Syndrome entered the conflict with latent Lyme disease. There has been no systematic examination of Gulf War Syndrome sufferers for chronic Lyme disease and it is hypothesized that chronic Lyme disease has been overlooked as a cause of Gulf War Syndrome. To address this it is suggested that sufferers of Gulf War Syndrome or similar illnesses should be examined by physicians who have experience diagnosing and treating large numbers of patients with Lyme disease.

Acute Peripheral Facial Palsy in Lyme Disease - A Distal Neuritis at the Infection Site

Children with acute peripheral facial palsy have often suffered tick bites and/or erythema migrans in the head/neck region on the same side. With respect to the pathogenesis of neuroborreliosis this topographical association was investigated in an animal model. A Borrelia garinii strain, isolated from the CSF of a child with acute facial palsy, was injected in 9 rats intracutaneously in the right subauricular region. Infected rats were examined for clinical symptoms of Lyme disease, the spread of the spirochetes was investigated by PCR of necropsies (facial nerves, trigeminus nerves, heart, brain, skin) up to 47 days after infection. The nerve tissues were investigated by histology, immunohistochemistry and electron microscopy. None of the rats developed a facial palsy or other symptoms of Lyme disease. Borrelia DNA was found in the heart after 5 days and in the brain after 7 days of infection up to the end of investigation (47 days), as well as in the ipsilateral peripheral nerves after 7 to 33 days. Borrelia was detected by electron microscopy near endoneural vessels of the facial nerve. Peri-, epi-, and endoneural infiltrations of macrophages, plasma cells and B cells characterized an inflammation of the facial and trigeminus nerves ipsilateral to the infection site. An infection with Borrelia garinii in the subauricular region induces an ipsilateral neuritis of peripheral nerves. The particular vulnerability of the human facial nerve may be a result of its long intraosseus course. Thus, an inflammatory edema may injure the nerve in the canalis facialis.

Emergency department management of Lyme disease

Lyme disease (LD), a vector-borne illness caused by Borrelia burgdorferi, has firmly entered the public consciousness since its initial description in 1977. Although it may be easily treated with antibiotics, perception of the threat LD poses far outweighs the actual medical sequelae endured by the 16,000 people annually affected in the United States. Of these, late neurologic, cardiac, and musculoskeletal complications are the most problematic. The recognition and treatment of early signs and symptoms of LD, especially erythema migrans (EM), is central to preventing the morbidity associated with late stages of LD. Because EM may be absent or subtle, familiarity with all of the manifestations of LD is essential for pediatric emergency medicine physicians.

Lyme disease—what is the cost for Scotland?

This paper analyses likely Lyme disease costs incurred by patients tested in the authors' laboratory over an 18 month period, based on patient histories and test results relating to 2110 samples submitted from laboratories serving 59% of the Scottish population. Cost analysis takes account of the direct costs of consultation, laboratory tests, antibiotic treatment and management of any sequelae, as well as indirect costs of the loss of healthy time through illness. Standard costs for each element are derived from published information, and the proportions applied to each patient category are estimated from studies described elsewhere in the literature. Of the sample, 295 patients had evidence of early Lyme disease and 31 had late Lyme disease symptoms. Based on these figures, the total annual cost for Lyme disease, when projected to the whole of Scotland, is estimated to be significant at £331,000 (range £47,000–615,000). The range is inevitably wide because it was not possible to document complete clinical and management histories on individual patients. In addition, some late Lyme disease sequelae will require management for more than 1 year, and costs are also identified that could justifiably be included for all the other patients who tested negative for Lyme disease. These data raise the question of whether there is sufficient focus on prevention and the best management of this disease.

Prevalence of IgG antibodies against Borrelia Burgdorferi s.l. and Ehrlichia Phagocytophila in sera of patients presenting symptoms of Lyme disease in a central region of Italy.

The aim of this study was to evaluate the prevalence (seroprevalence) of antibodies against Borrelia burgdorferi and Ehrlichia phagocytophila among patients resident in Lazio, a region of central Italy. Of a sample of 1,050 patients, which presented clinical manifestations related to Lyme disease, 34 (3.2%) were Borrelia-seropositive (Lyme index value >/= 1.2). The sera of 25 out of the 34 patients that were Borrelia-positive were also analysed for the presence of antibodies against E. phagocytophila and 3 (12%) were found Ehrlichia-positive (titres >1:64). No Ehrlichia positive samples were found among sera of 250 Borrelia-negative patients. Since both B. burgdorferi s.l. and Ehrlichia species share the same tick vector (Ixodes ricinus), our results indicate that concurrent transmission of these microbial pathogens might have been occurred among the patients included in this study.

Disease-specific diagnosis of coinfecting tickborne zoonoses: babesiosis, human granulocytic ehrlichiosis, and Lyme disease.

To determine whether a unique group of clinical and laboratory manifestations characterize certain major deer tick-transmitted human pathogens in North America, we compared the symptoms, short-term complications, and laboratory test results of New England residents who became ill due to > or =1 of these pathogens. Patients completed a uniformly structured questionnaire and submitted blood samples for serologic and polymerase chain reaction (PCR) testing after developing symptoms of Lyme disease, human babesiosis, or human granulocytic ehrlichiosis (HGE). Complete blood count with thin blood smear, PCR, and immunoglobulin M antibody tests helped differentiate the acute manifestations of these diseases. Physicians should consider use of tests designed to diagnose babesiosis and HGE in patients with Lyme disease who experience a prolonged flulike illness that fails to respond to appropriate antiborrelial therapy.

Laboratory testing for Lyme disease: possibilities and practicalities.

Lyme disease (LD) is a multisystem and multistage infection caused by three species of tick-borne spirochetes in the Borrelia burgdorferi sensu lato genogroup. These include B. burgdorferi sensu stricto (North America and Western Europe), Borrelia afzelii (Western Europe, Central Europe, and Russia), and Borrelia garinii (Europe, Russia, and northern Asia). LD has become the most common vector-borne disease in North America and Europe (5). In 1999, over 16,000 cases of human LD were reported in the United States by the Centers for Disease Control and Prevention (CDC), representing an overall incidence of 6.0 per 100,000 persons (9). Many cases go unreported in areas of endimicity; conversely, LD is probably overreported in some geographic areas where the disease is not known to be endemic. Like other spirochetal infections, the signs and symptoms of LD occur in stages and involve a variety of tissues and organs, including the skin, joints, heart, and nervous system. Early infection (stage 1) consists of primary erythema migrans (EM), an annular skin rash that begins days to weeks after a tick bite. Hematogenous dissemination of spirochetes over subsequent days to weeks (stage 2) can result in multiple skin lesions (secondary EM), as well as meningitis, radiculoneuritis, atrioventricular block, myocarditis, and oligoarticular arthritis. Persistent infection (stage 3) occurs months to years after the initial exposure and can be associated with acrodermatitis chronica atrophicans, varying degrees of encephalopathy and encephalomyelitis, and persistent arthritis. Of note, clinical manifestations of LD among patients in North America seem to differ somewhat from those residing in Europe and Asia. For example, acrodermatitis and severe encephalomyelitis due to LD are more common in Europe and Asia but are infrequent among patients in North America. These discrepancies can be explained, at least in part, by the different genospecies of Borrelia responsible for LD in various geographic areas and possibly by genetic differences among the affected populations (30). Recent reviews provide a comprehensive description of the clinical and epidemiologic aspects of LD (17, 21, 26). Since the initial description of Lyme arthritis 25 years ago, there have been tremendous gains in knowledge of the pathogenesis, epidemiology, diagnosis, and treatment of LD (29). The CDC has developed a case definition of LD for surveillance purposes that includes either physician-diagnosed EM along with solitary lesions with diameters of at least 5 cm or at least one late joint, neurologic, or cardiac manifestation along with laboratory confirmation (9). This definition is not intended to be 100% sensitive or specific for clinical diagnosis but is useful as a starting point for the development of a differential diagnosis and highlights the central role of laboratory testing, especially for extracutaneous LD. Laboratory tests have improved considerably over the above-mentioned time period, and clinicians now have available a wide, though somewhat bewildering, array of options for the direct detection of organisms in tissues, serologic detection of immune responses, and molecular detection of specific nucleic acid sequences and antigens. All of the various testing methodologies have their inherent advantages and limitations. It is extremely important to recognize that LD is a clinical diagnosis; any laboratory test used to supplement that evaluation should be ordered and interpreted in the context of careful investigation of the patient’s history and physical examination, i.e., after thoughtful assessment of the probability that a patient actually has a borrelial infection. This article reviews the various possibilities for LD testing and emphasizes some practicalities associated with the use of these tests given the present understanding of individual test performance.

Persistent Symptoms of Lyme Disease: Not Necessarily Responsive to Antibiotics

Late Lyme encephalopathy and neuropathy can be difficult to diagnose and manage. The encephalopathy usually is associated with impaired memory and

Persistence of immunoglobulin M or immunoglobulin G antibody responses to Borrelia burgdorferi 10-20 years after active Lyme disease.

The interpretation of serological results for patients who had Lyme disease many years ago is not well defined. We studied the serological status of 79 patients who had had Lyme disease 10-20 years ago and did not currently have signs or symptoms of active Lyme disease. Of the 40 patients who had had early Lyme disease alone, 4 (10%) currently had IgM responses to Borrelia burgdorferi, and 10 (25%) still had IgG reactivity to the spirochete, as determined by a 2-test approach (enzyme-linked immunosorbent assay and Western blot). Of the 39 patients who had had Lyme arthritis, 6 (15%) currently had IgM responses and 24 (62%) still had IgG reactivity to the spirochete. IgM or IgG antibody responses to B. burgdorferi may persist for 10-20 years, but these responses are not indicative of active infection.

Lyme disease and preventive behaviors in residents of Nantucket Island, Massachusetts

Background: To determine the age-specific prevalence of Lyme disease and whether preventive behaviors on Nantucket Island correlate with Lyme disease, we surveyed island residents. Methods: A survey with questions on Lyme disease symptoms, history, and preventive behaviors was mailed to all residents. Respondents were stratified by likelihood of having had Lyme disease. A subsample was selected for examination, and then classified according to the Lyme disease national surveillance case definition. Results: The overall lifetime prevalence of Lyme disease for Nantucket residents was 15% (CI, 10%–19.8%): 19% among females, and 11% among males. The prevalence was highest among age groups 0–16 and 30–49 years. Overall, 86% of the population practiced at least one behavior. The most frequently reported preventive behavior was checking oneself for ticks (80%), followed by wearing protective clothing (53%), avoiding tick areas (34%), and using tick repellent (11%). Younger individuals practiced fewer preventive behaviors than older individuals ( p=0.001). Although males reported greater tick exposure than females, females uniformly practiced preventive behaviors more frequently ( p=0.001). The practice of preventive behaviors was not associated with a history of Lyme disease, but finding more than 5 ticks per year on oneself was ( p=0.001). Conclusion: Lyme disease is highly prevalent on Nantucket Island. Young people are particularly at risk and health education should emphasize preventive behaviors less frequently practiced: using tick repellent, avoiding tick areas, and wearing protective clothing.

Decreased CD57 lymphocyte subset in patients with chronic Lyme disease

Background: Chronic Lyme disease (LD) is a debilitating illness caused by tickborne infection with the spirochete Borrelia burgdorferi. Although immunologic abnormalities appear to play a role in this disease, specific immunologic markers of chronic LD have not been identified. Methods: We evaluated 73 patients with chronic LD for lymphocyte subset abnormalities using flow cytometry. Of these, 53 patients had predominant musculoskeletal symptoms, while 20 patients had predominant neurologic symptoms. The estimated duration of infection ranged from 3 months to 15 years, and all patients had positive serologic tests for B. burgdorferi. Ten patients with acute LD (infection less than 1 month) and 22 patients with acquired immunodeficiency syndrome (AIDS) served as disease controls. Results: All 31 chronic LD patients who were tested prior to antibiotic treatment had significantly decreased CD57 lymphocyte counts (mean, 30±16 cells per μl; normal, 60–360 cells per μl, P<0.001). Nineteen of 37 patients (51%) who were tested after initiating antibiotic therapy had decreased CD57 levels (mean, 66±39 cells per μl), and all five patients tested after completing antibiotic treatment had normal CD57 counts (mean, 173±98 cells per μl). In contrast, all 10 patients with acute LD and 82% of AIDS patients had normal CD57 levels, and the difference between these groups and the pre-treatment patients with chronic LD was significant ( P<0.001). Patients with chronic LD and predominant neurologic symptoms had significantly lower mean CD57 levels than patients with predominant musculoskeletal symptoms (30±21 vs. 58±37 cells per μl, P=0.002). CD57 levels increased in chronic LD patients whose symptoms improved, while patients with refractory disease had persistently low CD57 counts. Conclusions: A decrease in the CD57 lymphocyte subset may be an important marker of chronic LD. Changes in the CD57 subset may be useful to monitor the response to therapy in this disease.

Antigenic conservation of an immunodominant invariable region of the VlsE lipoprotein among European pathogenic genospecies of Borrelia burgdorferi SL.

Lyme disease is caused by genetically divergent spirochetes, including 3 pathogenic genospecies: Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii. Serodiagnosis is complicated by this genetic diversity. A synthetic peptide (C(6)), based on the 26-mer invariable region (IR(6)) of the variable surface antigen of B. burgdorferi (VlsE), was used as ELISA antigen, to test serum samples collected from mice experimentally infected with the 3 genospecies and from European patients with Lyme disease. Regardless of the infecting strains, mice produced a strong antibody response to C(6), which indicates that IR(6) is antigenically conserved among the pathogenic genospecies. Twenty of 23 patients with culture-confirmed erythema migrans had a detectable antibody response to C(6). A sensitivity of 95.2% was achieved, with serum samples collected from patients with well-defined acrodermatitis chronica atrophicans. Fourteen of 20 patients with symptoms of late Lyme disease also had a positive anti-IR(6) ELISA. Thus, it is possible that C(6) may be used to serodiagnose Lyme disease universally.

Detection of borreliacidal antibodies in dogs after challenge with Borrelia burgdorferi-infected ixodes scapularis ticks.

Detection of borreliacidal antibodies is an accurate serodiagnostic test for confirmation of Lyme disease in humans. In this study, 13 pathogen-free beagles, 12 to 26 weeks old, were infected with Borrelia burgdorferi by tick challenge. Dogs were monitored for clinical signs and symptoms of Lyme disease along with borreliacidal antibody production against B. burgdorferi sensu stricto isolates 297 and 50772. Ten (77%) dogs developed lameness in one or more legs within 210 days after attachment of Ixodes scapularis ticks. Eight (80%) of the lame animals had concurrent fever of > or =38 degrees C. Spirochetes were also recovered from the skin and joints of 12 (92%) dogs, but rarely from other organs. Borreliacidal antibodies against B. burgdorferi isolate 297 were detected in only four (31%) dogs, and the levels of killing antibodies remained low for the duration of the infection. In contrast, borreliacidal antibodies against B. burgdorferi isolate 50772 were detected in 13 (100%) dogs within 21 days of infection. Furthermore, the borreliacidal antibody levels correlated with the severity of B. burgdorferi infection. Detection of borreliacidal antibodies, especially against B. burgdorferi isolate 50772, is also a reliable serodiagnostic test for detection of Lyme disease in dogs.

Soluble CD14 levels in the serum, synovial fluid, and cerebrospinal fluid of patients with various stages of Lyme disease.

Levels of circulating soluble CD14 (sCD14) in patients with various stages of Lyme disease (LD) were examined. Patients with early or untreated late LD had significantly higher levels of sCD14 than did healthy controls (P=.0001 and .0007, respectively); levels returned to normal within 3 months after antibiotic therapy. Patients with persistent posttreatment symptoms of LD had sCD14 levels equivalent to those of healthy controls. Differences in the serum sCD14 levels in patients with various stages of LD are likely to be directly correlated with differences in bacterial burden, suggesting that posttreatment symptoms may not require continued presence of the organism. sCD14 levels in the cerebrospinal fluid (CSF) of patients with any stage of LD were no different from those of control subjects. Levels of synovial fluid sCD14 from patients with Borrelia burgdorferi in their joints were elevated, compared with levels in normal serum, and may play a role in the pathogenesis of arthritis.