Neuroborreliosis with extrapyramidal symptoms: a case report.

 Pol Arch Med Wewn. 2008 May;118 5:314-7. : Neuroborreliosis with extrapyramidal
symptoms: a case report. Biesiada G, Czapiel J, Sobczyk-Krupiarz I, Garlicki A, Mach T.
Department of Infectious Diseases, Division of Gastroenterology, Hepatology, and Infectious 
Diseases, Jagiellonian University School of Medicine, Kraków, Poland.
The disease of Lyme is a tick-borne infection. It involves skin, the nervous system, joints and the 
heart. Spirochaeta Borrelia burgdorferi is the etiologic agent of the disease. In the majority of 
cases, clinical symptoms, like migrating erythema, occur from 3 to 30 days, sometimes to 3 
months after a bite from a tick. The early disseminated infection involves multiple migrating 
erythema, neuroborreliosis, arthritis, myocarditis and other organ-related symptoms. The late 
stage of chronic infection involves chronic atrophic leg dermatitis, neurological and 
rheumatological symptoms, and other organ-related symptoms which persist for above 12 
months. The diagnosis of the disease of Lyme is based upon specific clinical symptoms confirmed 
by serologic tests. The two-step diagnostic protocol including the ELISA method, confirmed by 
the Western-blot test, is optimal. The present article describes a case of a 59-year-old man, a 
computer specialist, who often spends his free time walking in woods for recreation, and who 
was bitten by a tick 3 years before hospitalization. The bite resulted in migrating erythema that 
subsided without antimicrobial treatment. In spite of this, the man had not changed his hobby 
exposing himself to bites from ticks. One year later, multiple migrating erythema and 
extrapyramidalis symptoms appeared without any other organ malfunctions. In the current 
year, the patient was admitted to the Infectious Diseases Hospital, and received antibiotics 
ceftriaxon with following neurological improvement. Several months later, extrapyramidal
symptoms increased. On the day of admission to the hospital, the neurologic examination 
showed abnormalities of upper and lower limbs movements propulsive walking and the right 
lower leg traction), the right hand tremor, pouts of the face, and sleepiness.
109:  1: J Neuroinflammation.  Sep 25;5:40. Persisting atypical and cystic forms of Borrelia
burgdorferi and local inflammation in Lyme neuroborreliosis. Miklossy J, Kasas S, Zurn AD, 
McCall S, Yu S, McGeer PL.
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC, 
BACKGROUND: The long latent stage seen in syphilis, followed by chronic central nervous 
system infection and inflammation, can be explained by the persistence of atypical cystic and 
granular forms of Treponema pallidum. We investigated whether a similar situation may occur in 
Lyme neuroborreliosis. METHOD: Atypical forms of Borrelia burgdorferi spirochetes were 
induced exposing cultures of Borrelia burgdorferi, strains B31 and ADB1, to such unfavorable 
conditions as osmotic and heat shock, and exposure to the binding agents Thioflavin S and 
Congo red. We also analyzed whether these forms may be induced in vitro, following infection of 
primary chicken and rat neurons, as well as rat and human astrocytes. We further analyzed 
whether atypical forms similar to those induced in vitro may also occur in vivo, in brains of three 
patients with Lyme neuroborreliosis. We used immunohistochemical methods to detect evidence 
of neuroinflammation in the form of reactive microglia and astrocytes. RESULTS: Under these 
conditions we observed atypical cystic, rolled and granular forms of these spirochetes. We 
characterized these abnormal forms by histochemical, immunohistochemical, dark field and 
atomic force microscopy, AFM, methods. The atypical and cystic forms found in the brains of 
three patients with neuropathologically confirmed Lyme neuroborreliosis were identical to those 
induced in vitro. We also observed nuclear fragmentation of the infected astrocytes using the 
TUNEL metho d. Abundant HLA-DR positive microglia and GFAP positive reactive astrocytes
were present in the cerebral cortex. CONCLUSION: The results indicate that atypical extra- 
and intracellular pleomorphic and cystic forms of Borrelia burgdorferi and local 
neuroinflammation occur in the brain in chronic Lyme neuroborreliosis. The persistence of 
these more resistant spirochete forms, and their intracellular location in neurons and glial
cells, may explain the long latent stage and persistence of Borrelia infection. The results also 
suggest that Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The detection 
and recognition of atypical, cystic and granular forms in infected tissues is essential for the 
diagnosis and the treatment as they can occur in the absence of the typical spiral Borrelia form

Leave a Reply

Your email address will not be published.