[Acute hepatitis in Lyme borreliosis].
The clinical feature of an acute hepatitis within a tick-borne meningopolyneuritis Garin-Bujadoux-Bannwarth is described by means of a given case and the etiological context is being discussed.
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Publications and source records attributed to G Stanek.
The clinical feature of an acute hepatitis within a tick-borne meningopolyneuritis Garin-Bujadoux-Bannwarth is described by means of a given case and the etiological context is being discussed.
In the course of routine gastroduodenoscopic examination of 218 patients bioptic mucosal specimens were examined bacteriologically for the presence of Campylobacter (C.) pylori. The organism was isolated from 52 out of 53 patients (98%) with duodenal ulcer, 7 out of 9 with gastric ulcer (78%), 24 out of 31 with mucosal erosions (77%), 10 out of 10 with duodenitis (100%), 16 out of 16 with chronic active gastritis (100%) and from 40 out of 73 patients (55%) with inactive chronic gastritis. By contrast, all specimens from 26 patients with endoscopically and histologically normal mucosa were negative for this bacterium. The rate of elimination of C. pylori from mucosal specimens was investigated as a first step towards studying the influence of antibiotic therapy upon healing of gastric and duodenal ulcers. For this purpose 30 patients with duodenal ulcers were treated either with ranitidine alone (15) or together with bacampicillin (15), which was shown to be highly active in studies with ampicillin in vitro. After 4 weeks the organism was still found in specimens from all patients treated with ranitidine alone, but also in 12 out of 15 patients given combined therapy. This result demonstrates that systemic antimicrobial chemotherapy with bacampicillin is insufficient to eradicate C. pylori from the stomach and the duodenum.
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A 19-year-old man developed chronic weakness of the lower limbs as the predominant manifestation of Borrelia burgdorferi infection of the nervous system. Spirochetes were demonstrated in the cerebrospinal fluid. The condition resolved following intravenous penicillin treatment.
During the 1982-1986 period of all bacterial pathogens found to have caused diarrhoea, 35% belonged to the genus Campylobacter (C). Approximately 70% of the strains were isolated from persons under the age of 30 years, with a distinct peak of occurrence in the autumn. Biotyping and serotyping according to Lior yielded the following results: C. jejuni biotype I: 32.9%, C. jejuni biotype II: 48.6%, C. coli biotype I: 10.3%, C. coli biotype II: 8.2%. From the 121 strains serotyped, 118 (97.5%) were typable. The serotypes most frequently encountered were type 1 (15.7%), 4 (9.9%), 2 and 11 (7.4% each). There were 2 familial outbreaks of Campylobacter enteritis which could be completely elucidated by biotyping and serotyping. One outbreak was caused by C. jejuni biotype I serotype 11, the other by C. jejuni biotype II serotype 6. Considering the frequent occurrence of Campylobacter infections, isolates should be routinely typed. The existing typing methods and schemes are highly developed.
Detection of intrathecally produced antibodies in cerebrospinal fluid (CSF) of patients with meningopolyneuritis Garin-Bujadoux-Bannwarth (MPN-GBB) is well documented. Analysis of CSF has revealed the oligoclonal nature of these antibodies. We investigated oligoclonal antibodies (OA) in CSF and serum of MPN-GBB patients with regard to immunoglobulin class, light chain type and specificity and compared the findings with those in other neurological diseases (OND). For this purpose an immunofixation (IF) technique after agarosegel electrophoresis (AE) of concentrated CSF was used. 87% of patients with MPN-GBB demonstrated in the acute stage of their disease oligoclonal bands (OB) in their CSF which could not be detected in paired serum samples. IF revealed in most cases of MPN-GBB IgG banding. While IgM banding was a common finding in CSF of MPN-GBB patients, this was not the case in OND. Specificity of CSF OA against components of Borrelia burgdorferi could be demonstrated by agarose isoelectric focusing (AIEF), transfer to nitrocellulose paper and reaction with 125I labelled B. burgdorferi antigen.
The cerebrospinal fluid (CSF) findings in 21 patients with different manifestations of Lyme disease are presented. 15 patients exhibited CSF changes including a lymphoplasmocytic pleocytosis and a CSF protein profile indicating a barrier leakage combined with an intrathecal immunoglobulin synthesis. Six patients-mainly suffering from cranial neuritis-had a normal CSF.
From January 1984 to August 1985 54 patients presented with cranial nerve lesions at the neurological department of the University hospital Innsbruck. Median age was 42 years, range 5-81 years. Female male ratio was 49/15. In 17 patients cranial neuritis was consistent with meningopolyneuritis Bannwarth (MPN) in 37 cases mere facial palsy was present. Cranial neuritis in MPN-patients affected N. facilis in 10, N. opticus and N. oculo-motorius in one case each. Five patients had polyneuritis cranialis with affection of the cranial nerves II, V, VI, VII, VIII, and IX (Table 1). IgG-antibodies to B. burgdorferi were found in the sera of all MPN patients and in 15 of cases with mere facial palsy. Patients with antibodies to B. burgdorferi were treated with intravenous penicillin and latamoxef dinatrium. The remaining 22 patients were treated with vitamin B compound and corticosteroids. The time for full recovery was 4 weeks on the average in each treatment group.
We report on the clinical symptoms of 50 patients with serologically proven B. burgdorferi infection in stage 2 Lyme disease. Besides the typical pattern of the GBB-syndrom myelitis, encephalitis, cranial nerve neuritis others than Bell's palsy, painful neuritis without CSF-pleocytosis and meningitis without other neurological findings were observed.
Clinical data of 19 patients with meningopolyneuritis Garin-Bujadoux-Bannwarth (MPN-GBB), treated with 2 X 10 million units intravenous sodium penicillin for 10 days, were evaluated at the beginning of therapy, 3 weeks thereafter, and 6 months after onset of the neurological disease. Cerebrospinal fluid (CSF) was analysed in 14 patients at the onset of therapy and 3 1/2 weeks thereafter. At the same interval antibodies against B. burgdorferi were measured by enzyme-linked immunosorbent assay (ELISA) in the CSF and sera of 12 patients. Clinical data and all CSF results, with exception of specific antibody titers, were compared with those of patients who had suffered from MPN-GBB between 1979 and 1983, and who had not received antibiotic or corticosteroid therapy. Comparing the clinical data of all treated patients with those of all non-treated controls, no significant difference could be observed. A significant improvement could however be detected in those patients who had their treatment begun 5 weeks within onset of the neurological disease. Changes in CSF 3 1/2 weeks after onset of treatment showed slight differences when compared with controls.
72 patients with Erythema chronicum migrans were treated with phenoxymethyl penicillin, 1,5 mill. IU p.o. three times a day for 14 days. Two children got the same therapy, but in a dosage of 400,000 IU three times a day for 10 days. In three of 15 skin samples, taken from the periphery of ECM lesions, spirochetal organisms were isolated. Of the 72 patients 16 had raised IgG (greater than or equal to 128) and 9 had raised IgM (greater than or equal to 64) titers to Borrelia burgdorferi. Under treatment with phenoxymethyl penicillin (penicillin V) all ECM lesions resolved within 6 to 10 days. After an observation period of 9 to 14 months no major or minor late manifestations of Lyme disease have developed in any of the 72 patients.
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From April 1984 to July 1985 873 cases of Borrelia infections were registered at the Hygiene Institute of the University of Vienna. 2609 serum samples of these patients were investigated for antibodies against B. burgdorferi by means of IFA- and ELISA-tests. Erythema chronicum migrans (ECM) was recognized in 60.9% of patients, neurological abnormalities were recorded in 23.4% of which the majority manifested themselves as polyradiculitis and meningopolyneuritis (MPN). Acrodermatitis chronica atrophicans (ACA) was recognized in 11.5%. A small number of patients suffered from Lymphadenosis cutis benigna (LCB), arthritis and cardiac abnormalities. Sixty percent of patients were females and 40% males. Infections were found in all age groups ranging from 2-83 years in females and 1-85 years in males. Tick- or insect-bites prior to the onset of illness were reported by 47.2% and 15.6% of patients, respectively. The main vector is the hard tick Ixodes ricinus. Flying insects from the family tabanidae, i.e. Chrysops caecutiens and Haematopota species, must also be considered as transmitters. Antibodies to B. burgdorferi were found in 22.3%, 93.6% and 100% of sera from patients with ECM, MPN and ACA, respectively. Six of 11 patients with LCB and all with arthritis and cardiac abnormalities showed serologic reactivity. Geographically, Borrelia infections are distributed in all states of Austria. The seasonal distribution of cases show a peak in July and August, but the onset of clinical manifestation could be observed throughout the year. These results present Austria as an area where tick- or insect-borne Borrelia infections are very frequent and endemic in all Austrian states.
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In order to elucidate the possible spirochetal origin of morphea and lichen sclerosus et atrophicans (LSA), we investigated biopsy specimens from 13 patients with morphea and 13 patients with LSA. Four patients with acrodermatitis chronica atrophicans (ACA), three with erythema chronicum migrans (ECM), and 11 patients with other inflammatory dermatoses served as controls. Formalin-fixed, paraffin-embedded sections were stained by an avidin-biotin-immunoperoxidase method, using serum of a patient with ACA that contained IgG antibodies to Borrelia burgdorferi. As positive control substrate, formalin-fixed culture suspensions of B. burgdorferi strain B31 were used. They presented either as thin, mostly linear, but partially dotted, stained spirochetes or, in contrast, as thick, "swollen," heavily stained organisms. Identical structures could also be detected on histological sections of one patient with ECM, four patients with morphea, and six patients with LSA. These findings provide evidence for the spirochetal origin of both morphea and LSA.
Three European patients had chronic active forms of Borrelia burgdorferi infection of the nervous system, with high titers of antibodies to this spirochete in serum and CSF. Two patients had meningitis for 3 to 4 years, with remissions in one and slowly progressive symptoms in the other. Both had CT lucencies in the basal ganglia. The third patient had lumbosacral plexus neuropathy for 1 year. All three patients responded to intravenous penicillin treatment.