Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis

Miklóssy, Judith; Küntzer, Thierry; Bogousslavsky, J; Régli, F; Janzer, Robert-Charles

doi:10.1007/bf00294622

Cited by 62 publications

(44 citation statements)

References 16 publications

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“…The meningovascular lesions in our case arc compat ible with LNB pathology [11], In contrast the spongiform change in the cerebral cortex and thalamus has not been reported. The spongy areas were covered with numerous activated microglial cells and GFAP-positive astrocytes, and absence of neurons showing ischemic change ex cludes a possibility of systemic hypoxia.…”

Section: Discussionmentioning

confidence: 69%

“…Pachner et al [8] reported 6 patients with LNB and a brain biopsy specimen taken from 1 patient with chronic encephalopa thy demonstrated microglial nodules and silver-impreg nated organisms without any necrotic lesion or perivascu lar lymphocyte infiltration. Miklossy et al [11] demon strated a brain that showed meningitis and multiple isch emic lesions caused by occlusive vascular change with perivascular leukocyte infiltration, and they concluded that the parenchymal CNS lesions were ischemic infarcts due to occlusive vascular changes and meningitis, both of which were consistent with those in meningovascular forms of tertiary neurosyphilis. In a most recent study, Oksi et al [ 15] reported a necropsied brain infected con comitantly with thick-borne virus and B. burgdorferi, in which hemorrhagic necroses of the bilateral hippocampi, glial nodules and neuronal cell loss in the thalamus, cere bral cortex and spinal cord were found.…”

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confidence: 72%

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<i>Borrelia burgdorferi</i>-Seropositive Chronic Encephalomyelopathy: Lyme Neuroborreliosis?

Kobayashi

Mizukoshi

Aoki

et al. 1997

Dement Geriatr Cogn Disord

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A 36-year-old Japanese woman presented with progressive cerebellar signs and mental deterioration of subacute course after her return from the USA. Her serum antibody to spirochete Borrelia burgdorferi was significantly elevated. A necropsy 4 years after her initial neurological signs revealed multifocal inflammatory change in the cerebral cortex, thalamus, superior colliculus, dentate nucleus, inferior olivary nucleus and spinal cord. The lesions showed spongiform change, neuronal cell loss, astrocytosis and proliferation of activated microglial cells. The internal capsule was partially vacuolated and the spinal cord, notably at the thoracic level, was demyelinated and cavitated in the lateral funiculus. Microglial cells aggregated within and around the spongiform lesions and microglial nodules were present in the medulla oblongata. Use of Warthin-Starry stain demonstrated silver-impregnated organisms strongly suggesting B. burgdorferi in the central nervous tissues. The dentate nucleus and inferior olivary nucleus showed the most advanced lesions with profound fibrillary gliosis. Occlusive vascular change was relatively mild, and fibrous thickening of the leptomeninges with lymphocyte infiltrates was localized in the basal midbrain. The ataxic symptoms were due to the dentate and olivary nucleus lesions and mental deterioration was attributable to the cortical and thalamic lesions. Spongiform change, neuronal cell loss, and microglial activation are characteristic pathological features in the present case. The cerebellar ataxia and subsequent mental deterioration are unusual clinical features of Lyme neuroborreliosis. Spirochete B. burgdorferi can cause focal inflammatory parenchymal change in the central nervous tissues and the present case may be an encephalitic form of Lyme neuroborreliosis.

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Section: Discussionmentioning

confidence: 69%

mentioning

confidence: 72%

<i>Borrelia burgdorferi</i>-Seropositive Chronic Encephalomyelopathy: Lyme Neuroborreliosis?

Kobayashi

Mizukoshi

Aoki

et al. 1997

Dement Geriatr Cogn Disord

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“…obliterative inflammatory vasculopathy associated with spirochetes present in the leptomeninges, have been described as ‘a meningovascular form of neuroborreliosis’ [22]. In syphilis, obliterative endarteritis of the vasa vasorum of large arteries can lead to aneurysm formation [23].…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vasculitis and Stroke in Lyme Neuroborreliosis

Topakian¹,

Stieglbauer²,

Nußbaumer³

et al. 2008

Cerebrovasc Dis

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We report on 2 patients with cerebral vasculitis and stroke due to Lyme neuroborreliosis (LNB). Both patients had a prodromal stage involving headaches, and showed meningeal enhancement in addition to ischemic infarctions on brain magnetic resonance imaging and diffuse vasculitis on vascular imaging. Serological and cerebrospinal (CSF) fluid studies confirmed the diagnosis of active LNB. Ceftriaxone for 3 weeks led to an excellent recovery and improvements in the CSF examination findings. Stroke physicians should be aware of this rare presentation of LNB. A review of the current knowledge on cerebral vasculitis due to LNB is provided.

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“…The most common manifestations of Lyme neuroborreliosis are headache, meningismus, or radiculopathic symptoms, whereas CNS parenchymal involvement is rare (Hansen and Lebech, 1992;Pacher et al, 1998a). The localization of spirochetes in the CNS of humans has been reported only in a handful of cases using nonspecific silver impregnation techniques (Kobayashi et al, 1997;Kuntzer et al, 1991;Miklossy et al, 1990). The positivity of the PCR-ELISA in samples from the cerebrum and brainstem likely represents leptomeningeal, rather than parenchymal, localization.…”

Section: Borrelia Burgdorferi In Immunosuppressed Macaca Mulattamentioning

confidence: 99%

Localization of Borrelia Burgdorferi in the Nervous System and Other Organs in a Nonhuman Primate Model of Lyme Disease

Cadavid

O'Neill

Schaefer

et al. 2000

Laboratory Investigation

112

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SUMMARY:Lyme borreliosis is caused by infection with the spirochete Borrelia burgdorferi. Nonhuman primates inoculated with the N40 strain of B. burgdorferi develop infection of multiple tissues, including the central (CNS) and peripheral nervous system. In immunocompetent nonhuman primates, spirochetes are present in low numbers in tissues. For this reason, it has been difficult to study their localization and changes in expression of surface proteins. To further investigate this, we inoculated four immunosuppressed adult Macaca mulatta with 1 million spirochetes of the N40 strain of B. burgdorferi, and compared them with three infected immunocompetent animals and two uninfected controls. The brain, spinal cord, peripheral nerves, skeletal muscle, heart, and bladder were obtained at necropsy 4 months later. The spirochetal tissue load was first studied by polymerase chain reaction (PCR)-ELISA of the outer surface protein A (ospA) gene. Immunohistochemistry was used to study the localization and numbers of spirochetes in tissues and the expression of spirochetal proteins and to characterize the inflammatory response. Hematoxylin and eosin and trichrome stains were used to study inflammation and tissue injury. The results showed that the number of spirochetes was significantly higher in immunosuppressed animals. B. burgdorferi in the CNS localized to the leptomeninges, nerve roots, and dorsal root ganglia, but not to the parenchyma. Outside of the CNS, B. burgdorferi localized to endoneurium and to connective tissues of peripheral nerves, skeletal muscle, heart, aorta, and bladder. Although ospA, ospB, ospC, and flagellin were present at the time of inoculation, only flagellin was expressed by spirochetes in tissues 4 months later. Significant inflammation occurred only in the heart, and only immunosuppressed animals had cardiac fiber degeneration and necrosis. Plasma cells were abundant in inflammatory foci of steroid-treated animals. We concluded that B. burgdorferi has a tropism for the meninges in the CNS and for connective tissues elsewhere in the body. (Lab Invest 2000, 80:1043-1054.

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Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis

Cited by 62 publications

References 16 publications

<i>Borrelia burgdorferi</i>-Seropositive Chronic Encephalomyelopathy: Lyme Neuroborreliosis?

<i>Borrelia burgdorferi</i>-Seropositive Chronic Encephalomyelopathy: Lyme Neuroborreliosis?

Cerebral Vasculitis and Stroke in Lyme Neuroborreliosis

Localization of Borrelia Burgdorferi in the Nervous System and Other Organs in a Nonhuman Primate Model of Lyme Disease

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