- Acta Neurol Scand. 2007 Feb;115(2):129-31.
Motor neuron disease recovery associated with IV ceftriaxone and anti-Babesia therapy.
Harvey WT, Martz D.
Rocky Mountain Chronic Disease Specialists, L.L.C., North Circle Drive, Colorado Springs, CO 80909, USA. [email protected]
Comment in: Acta Neurol Scand. 2008 Mar;117(3):217.
This report summarizes what we believe to be the first verifiable case of a significant and progressive motor neuron disease (MND) consistent with amyotrophic lateral sclerosis that resolved during treatment with i.v. ceftriaxone plus oral atovaquone and mefloquine. The rationale for use of these antibiotics was (i) positive testing for Borrelia burgdorferi and (ii) red blood cell ring forms consistent with Babesia species infection. The patient has continued to be free of MND signs and symptoms for 15 months, although some symptoms consistent with disseminated Borreliosis remain.
PMID: 17212618 [PubMed - indexed for MEDLINE]
- Int J Health Geogr. 2002 Dec 20;1(1):5.
Geographical and seasonal correlation of multiple sclerosis to sporadic schizophrenia.
Clinic for Internal Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland. [email protected]
BACKGROUND: Clusters by season and locality reveal a striking epidemiological overlap between sporadic schizophrenia and multiple sclerosis (MS). As the birth excesses of those individuals who later in life develop schizophrenia mirror the seasonal distribution of Ixodid ticks, a meta analysis has been performed between all neuropsychiatric birth excesses including MS and the epidemiology of spirochaetal infectious diseases. RESULTS: The prevalence of MS and schizophrenic birth excesses entirely spares the tropical belt where human treponematoses are endemic, whereas in more temperate climates infection rates of Borrelia garinii in ticks collected from seabirds match the global geographic distribution of MS. If the seasonal fluctuations of Lyme borreliosis in Europe are taken into account, the birth excesses of MS and those of schizophrenia are nine months apart, reflecting the activity of Ixodes ricinus at the time of embryonic implantation and birth. In America, this nine months' shift between MS and schizophrenic births is also reflected by the periodicity of Borrelia burgdorferi transmitting Ixodes pacificus ticks along the West Coast and the periodicity of Ixodes scapularis along the East Coast. With respect to Ixodid tick activity, amongst the neuropsychiatric birth excesses only amyotrophic lateral sclerosis (ALS) shows a similar seasonal trend. CONCLUSION: It cannot be excluded at present that maternal infection by Borrelia burgdorferi poses a risk to the unborn. The seasonal and geographical overlap between schizophrenia, MS and neuroborreliosis rather emphasises a causal relation that derives from exposure to a flagellar virulence factor at conception and delivery. It is hoped that the pathogenic correlation of spirochaetal virulence to temperature and heat shock proteins (HSP) might encourage a new direction of research in molecular epidemiology.
PMCID: PMC149400 PMID: 12537588 [PubMed - as supplied by publisher]
- Rev Neurol. 1997 Dec;25(148):1919-21.
[Neuroborreliosis in a patient with progressive supranuclear paralysis. An association or the cause?]
[Article in Spanish]
García-Moreno JM, Izquierdo G, Chacón J, Angulo S, Borobio MV.
Departamento de Inmunología, Hospital Universitario Virgen de la Macarena, Sevilla, España. [email protected]
INTRODUCTION: Many different neurological conditions may be seen in the later stages of Lyme's Disease, such as blindness, epileptic crises, CVA, extrapyramidal disorders, amyotrophic lateral sclerosis, and dementia may be yet another form of presentation of chronic infection due to Borrelia burgdorferi (Bb). Progressive Supranuclear Paralysis (PSP), a disorder of unknown aetiology, considered to be the commonest cause of Parkinsonism-plus, one of the symptoms of which is dementia, has never been mentioned in this type of differential diagnosis. CLINICAL CASE: We present the case of a 78 year old man with sub-acute mental deterioration, Bb positive serology in both plasma and CSF, and with clinical and epidemiological features compatible with Lyme's Disease. Complementary tests were negative. The syndrome corresponded to Lyme's Disease and improved after treatment with ceftriaxona. CONCLUSIONS: We consider aspects of the aetiology of PSP which are still not clear. In our patient, the aetiology seemed to be Bb infection, according to the criteria of the original description of the disease and in view of the neuropathological findings which have shown Bb in the substancia nigra of the mid-brain and the existence of an animal model in which Bb shows a particular tendency to colonize infratentorial structures.
PMID: 9528031 [PubMed - indexed for MEDLINE]
- Wien Med Wochenschr. 1995;145(7-8):186-8.
[ALS-like sequelae in chronic neuroborreliosis]
[Article in German]
Hänsel Y, Ackerl M, Stanek G.
Neurologischen Abteilung des Kaiser-Franz-Josef-Spitals, Wien.
CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.
PMID: 7610670 [PubMed - indexed for MEDLINE]
- Neurologia. 1994 Jan;9(1):29-31.
[Failure of empirical treatment with ceftriaxone in motor neuron disease]
[Article in Spanish]
Carod Artal FJ, Pérez López-Fraile I, Gracia Naya M, Girón Mombiela JA.
Servicio de Neurología, Hospital Miguel Servet, Zaragoza.
Comment in: Neurologia. 1994 May;9(5):205-6.
We describe two patients with lateral amyotrophic sclerosis who, after informed consent, received empirical treatment with intravenous cephtriaxone at a dose of 2 g/24 hours for three weeks, with no positive results. The pharmacokinetics of this cephalosporin is analyzed, along with the relationship between motor neuron disease, neuroborreliosis and immunoreactivity to Borrelia burgdorferi.
PMID: 8161465 [PubMed - indexed for MEDLINE]
- J Clin Microbiol. 1990 Jun;28(6):1329-37.
Reactivity of human Lyme borreliosis sera with a 39-kilodalton antigen specific to Borrelia burgdorferi.
Simpson WJ, Schrumpf ME, Schwan TG.
Arthropod-borne Diseases Section, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.
Borrelia burgdorferi is the causative agent of Lyme borreliosis, a spirochetal illness with a variety of acute clinical manifestations that may lead to debilitating neurological and arthritic complications. Diagnosis is difficult because symptoms mimic a variety of unrelated clinical conditions, spirochetes cannot always be isolated from infected patients, and current serological tests are frequently inconclusive because of the presence of cross-reacting non-B. burgdorferi antibodies. To identify antigens specific to B. burgdorferi that could be used in the serodiagnosis of Lyme borreliosis, we screened a Borrelia DNA expression library in Escherichia coli for antigens reactive with human Lyme borreliosis sera. One clone carried a 6.3-kilobase EcoRI chromosomal fragment (pSPR33), which encoded two species-specific antigens with molecular masses of 28 (P28) and 39 (P39) kilodaltons (kDa). These two antigens were immunologically distinct from OspA, OspB, and the 41-kDa flagellin. Ninety-four serum specimens from patients having Lyme borreliosis were tested for reactivity with P39. All of 33 the serum specimens with immunofluorescence assay titers of greater than or equal to 1:256, 13 of 17 serum specimens with titers of 1:128, and 14 of 44 serum specimens with titers of less than or equal to 1:64 reacted with P39. Notably, many sera reactive to P39 did not appear to react with the 41-kDa flagellin. Therefore, antibody to P39 could be mistaken for antibody to the 41-kDa flagellin in tests of human sera by Western blot (immunoblot). Twenty-five control serum specimens, which included sera from syphilitic, relapsing fever, and amyotrophic lateral sclerosis patients as well as from 10 normal individuals, did not react to P39. Our data suggest that P39 may be a useful antigen for the serological confirmation of Lyme borreliosis.
PMCID: PMC267928 PMID: 2380361 [PubMed - indexed for MEDLINE]
- Arch Neurol. 1990 May;47(5):586-94.
Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease.
Halperin JJ, Kaplan GP, Brazinsky S, Tsai TF, Cheng T, Ironside A, Wu P, Delfiner J, Golightly M, Brown RH, et al.
Department of Neurology, State University of New York, Stony Brook 11794.
Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi; 4 of 38 matched controls were seropositive. Eight of 9 seropositive patients were male (8 of 12 male patients vs 2 of 24 controls). Rates of seropositivity were lower among patients with ALS from nonendemic areas. All patients had typical ALS; none had typical Lyme disease. Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti-B burgdorferi antibody. Following therapy with antibiotics, 3 patients with predominantly lower motor neuron abnormalities appeared to improve, 3 with severe bulbar dysfunction deteriorated rapidly, and all others appeared unaffected. There appears to be a statistically significant association between ALS and immunoreactivity to B burgdorferi, at least among men living in hyperendemic areas.
PMID: 2334308 [PubMed - indexed for MEDLINE]
- N Engl J Med. 1989 Jan 26;320(4):255-6.
Lack of antibodies to Borrelia burgdorferi in patients with amyotrophic lateral sclerosis.
Mandell H, Steere AC, Reinhardt BN, Yoshinari N, Munsat TL, Brod SA, Clapshaw PA.
PMID: 2911315 [PubMed - indexed for MEDLINE]
- Lancet. 1987 Aug 8;2(8554):332-3.
Borrelia burgdorferi antibodies and amyotrophic lateral sclerosis.
Waisbren BA, Cashman N, Schell RF, Johnson R.
PMID: 2886788 [PubMed - indexed for MEDLINE]