scholarly journals Early Disseminated Lyme Disease with Carditis Complicated by Posttreatment Lyme Disease Syndrome

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Cheryl Novak ◽  
Andrew Harrison ◽  
John Aucott

Lyme disease is an infectious disease caused by the bacterium Borrelia burgdorferi. When untreated, infection may spread to the heart, nervous system, and joints. Cardiac involvement usually manifests as abnormalities of the conduction system and bradycardia. Treatment of Lyme disease is generally effective, with a subset of patients experiencing persistent, sometimes long-term symptoms called posttreatment Lyme disease syndrome.

Author(s):  
L. P. Melnyk ◽  
L. A. Hryshchuk ◽  
M. Koziol–Montewka ◽  
P. S. Tabas ◽  
R. O. Klos

Background. Lyme disease has many clinical features similar tothose in sarcoidosis and tuberculosis. Epidemiological data in the world, in particular in Ukraine, proves the increase in Lyme borreliosis incidence. Ternopil region is endemic with Lyme borreliosis.Objective. The research was aimed to investigate the prevalence of infection with Borrelia burgdorferi and epidemiology features of borreliosis among the patients of Ternopil Regional TB Dispensary.Methods. In total, 29 patients were admitted to Departments of Differential Diagnostic, TB Therapy and TB Surgery of Ternopil Regional TB Dispensary in October 2016-January 2017. All the surveyed answered the questions of an integrated international questionnaire, where they noted the area and a number of tick bites, described the removal method, noted the survey for borreliosis pathogen and complaints after tick bites.Results. It was established that 5 respondents had a history of tick bites episodes, but only in one case the patient was examined of borreliosis. Tick bites were noticed in 3 patients with sarcoidosis and 1 with tuberculosis (TB) and exudative pleurisy, respectively.Conclusions. The absence of appeals for medical care, lack of sufficient information on Lyme borreliosis and disuse of preventive measures for tick bites by the interviewed patients of Ternopil regional TB dispensary departments proves the need of improvement of health education on Lyme borreliosis (LB) among this category of population. 24 (82.7%) of 29 respondents did not remember the tick bite. The symptoms of (LB) are similar to those in sarcoidosis and tuberculosis (pleural lesions, heart, joints, nervous system, skin), and the presence of tick bites gives the reasons to examine these patients of Borrelia burgdorferi senso lato.


Author(s):  
John J. Halperin

Nervous system involvement occurs in 10% to 15% of patients infected with Borrelia burgdorferi, B. afzelii, or B. garinii, the tick-borne spirochetes responsible for Lyme disease and its European counterparts. Common clinical manifestations include lymphocytic meningitis, facial and other cranial neuropathies, and painful mononeuropathies such as Lyme radiculitis. Diagnosis requires appropriate clinical, epidemiological, and laboratory evidence. Appropriately interpreted serologic testing is highly reliable; cerebrospinal fluid examination is often informative if the central nervous system is involved. Several week courses of widely available oral or parenteral antimicrobials are curative in most patients.


2020 ◽  
Author(s):  
Timothy Casselli ◽  
Ali Divan ◽  
Yvonne Tourand ◽  
Heidi L. Pecoraro ◽  
Catherine A. Brissette

ABSTRACTLyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, and nervous systems including the central nervous system (CNS). Inbred laboratory mice are effective models for characterizing B. burgdorferi infection kinetics and host immune responses in joints and heart tissues; however, similar studies are lacking in the CNS of these animals. Here we characterize the kinetics of B. burgdorferi colonization and associated immune responses in the CNS of infected C3H mice during early and subacute infection. B. burgdorferi colonized the dura mater following needle or tick challenge, and induced expression of inflammatory cytokines and a robust IFN response as well as histopathological changes. A sterile IFN response in the absence of B. burgdorferi or inflammatory cytokines was unique to the brain parenchyma, and could provide insights into the mechanism of inflammatory CNS pathology associated with this important pathogen.


2019 ◽  
pp. 321-328 ◽  
Author(s):  
Katarzyna Krawczuk ◽  
Piotr Czupryna ◽  
Sławomir Pancewicz ◽  
Elżbieta Ołdak ◽  
Monika Król ◽  
...  

Neuroborreliosis is one of the manifestations of Lyme disease involving central and peripheral nervous system. It is caused by infection with Borrelia burgdorferi spirochete which is transmitted by tick bites. Neuroborreliosis can affect both adults and children. The clinical course in children is often different than in adults. The article discusses the most common clinical symptoms, complications, diagnostics and treatment of neuroborreliosis in children.


2020 ◽  
Vol 21 (5) ◽  
pp. 517-526
Author(s):  
Manzama-Esso Abi ◽  
Zhenhua Ji ◽  
Miaomiao Jian ◽  
Xiting Dai ◽  
Ruolan Bai ◽  
...  

Lyme disease (LD) is an infectious disease caused by the spirochetes of genus borrelia, which are transmitted by the ticks of the genus ixodes. LD is transmitted by the spirochete B. burgdorferi sensu lato. Once in contact with the host through a tick bite, the pathogen comes into contact with the host defense, and must escape this machinery to establish LD, thus using a large number of mechanisms involving the vector of the pathogen, the pathogen itself and also the host. The initial diagnosis of the disease can be made based on the clinical symptoms of LD and the disease can be treated and cured with antibiotics if the diagnosis is made early in the beginning of the disease. Contrariwise, if LD is left untreated, the pathogen disseminates throughout the tissues and organs of the body, where it establishes different types of disease manifestations. In the nervous system, the inflammation caused by B. burgdorferi is known as Lyme neuroborreliosis (LNB). LNB is one of the principal manifestations of LD. In this review, we systematically describe the different molecular interactions among B. burgdorferi, the vector (tick) and the mammalian host.


2019 ◽  
Vol 30 (5) ◽  
pp. NP46-NP52
Author(s):  
Lucia Mata-Moret ◽  
Carolina Garcia-Villanueva ◽  
Clara Monferrer-Adsuara ◽  
Veronica Castro Navarro ◽  
Enrique Cervera-Taulet

Lyme disease is a rare condition caused by the bacterium Borrelia burgdorferi. Despite typical symptoms including fever, headache, fatigue, and a characteristic skin rash, sometimes we cannot find those due to the lack of physician consultation in those early stages. If this disease is left untreated, infection could spread to the nervous system causing neuroborreliosis, an atypical and complicated manifestation of this disease. We present the case of an atypical papillitis, probably caused by this bacterium. We suspected this because of the results on the indirect test bloods and the improvement of the symptoms after treatment. This entity should be considered as a possible diagnosis of atypical optical neuropathies, particularly if it occurs in an endemic area.


2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Geetha Parthasarathy ◽  
Shiva Kumar Goud Gadila

AbstractEven after appropriate treatment, a proportion of Lyme disease patients suffer from a constellation of symptoms, collectively called Post-Treatment Lyme Disease Syndrome (PTLDS). Brain PET scan of patients with PTLDS have demonstrated likely glial activation indicating persistent neuroinflammatory processes. It is possible that unresolved bacterial remnants can continue to cause neuroinflammation. In previous studies, we have shown that non-viable Borrelia burgdorferi can induce neuroinflammation and apoptosis in an oligodendrocyte cell line. In this follow-up study, we analyze the effect of sonicated remnants of B. burgdorferi on primary rhesus frontal cortex (FC) and dorsal root ganglion (DRG) explants. Five FC and three DRG tissue fragments from rhesus macaques were exposed to sonicated B. burgdorferi and analyzed for 26 inflammatory mediators. Live bacteria and medium alone served as positive and negative control, respectively. Tissues were also analyzed for cell types mediating inflammation and overall apoptotic changes. Non-viable B. burgdorferi induced significant levels of several inflammatory mediators in both FC and DRG, similar to live bacteria. However, the levels induced by non-viable B. burgdorferi was often (several fold) higher than those induced by live ones, especially for IL-6, CXCL8 and CCL2. This effect was also more profound in the FC than in the DRG. Although the levels often differed, both live and dead fragments induced the same mediators, with significant overlap between FC and DRG. In the FC, immunohistochemical staining for several inflammatory mediators showed the presence of multiple mediators in astrocytes, followed by microglia and oligodendrocytes, in response to bacterial remnants. Staining was also seen in endothelial cells. In the DRG, chemokine/cytokine staining was predominantly seen in S100 positive (glial) cells. B. burgdorferi remnants also induced significant levels of apoptosis in both the FC and DRG. Apoptosis was confined to S100 + cells in the DRG while distinct neuronal apoptosis was also detected in most FC tissues in response to sonicated bacteria. Non-viable B. burgdorferi can continue to be neuropathogenic to both CNS and PNS tissues with effects likely more profound in the former. Persistence of remnant-induced neuroinflammatory processes can lead to long term health consequences.


2000 ◽  
Vol 31 (5) ◽  
pp. 1149-1154 ◽  
Author(s):  
T. J. Wang ◽  
M. H. Liang ◽  
O. Sangha ◽  
C. B. Phillips ◽  
R. A. Lew ◽  
...  

2006 ◽  
Vol 75 (1) ◽  
pp. 243-251 ◽  
Author(s):  
Jan D. Lünemann ◽  
Harald Gelderblom ◽  
Mireia Sospedra ◽  
Jacqueline A. Quandt ◽  
Clemencia Pinilla ◽  
...  

ABSTRACT 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.


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