[Guidelines followed criticism concerning truth disclosure when it comes to cancer via telephone].
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Biomedical subjects
Publications and source records attributed to B E Malmvall.
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To clarify whether a nosocomial outbreak of legionnaires' disease in the Värnamo hospital in Sweden was part of a wider outbreak in the Värnamo community a number of investigations were performed. First, the proportion of cases of legionnaires' disease in a group with nosocomially acquired pneumonia (11%) was compared to the proportion within a group with community-acquired pneumonia (14%) and the difference was found not to be significant (p > 0.05). Second, the proportion of the nursing staff at the Värnamo hospital with an elevated antibody titre (> or = 16) to Legionella pneumophila serogroup (sg) 1 (33%, 84/258) was compared to the proportion in a group of local residents of Värnamo community (26%, 25/96) and found not to be significant; in contrast, comparison with the proportion in a group from the assistant nursing staff at another hospital 60 km away (5%, 4/80) was highly significant (p < 0.001). Furthermore, Legionella species were cultured from samples drawn from the hospital water supply as well from the water supply from municipal buildings. In 1996 a follow-up study was conducted, which showed that < 1% of the assistant nurses and local residents had an elevated titre to L. pneumophila sg 1. These results indicate that there was a temporary spread of L. pneumophila sg 1 in the Värnamo community at the beginning of 1991, both in the local hospital and the surrounding community. This implies that physicians should be aware of community-acquired cases of legionnaires' disease when a nosocomial outbreak is detected.
Whereas giant cell arteritis (GCA) was considered a rare disease 50 years ago, the generalized arteritis is now recognized as an important and significant cause of morbidity in elderly people; its cause and pathogenesis is poorly understood. Glucocorticosteroids are the drug of choice in all clinical types of GCA. In contrast to corticosteroids, nonsteroidal anti-inflammatory drugs have no proven effect on vascular complications to GCA, and cannot be recommended.
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We report a nosocomial outbreak of Legionella pneumophila serogroup (sg) 1 infection at the general hospital, Värnamo, Sweden. From December 1990 to February 1991, 28 patients and 3 staff fell ill with pneumonia and 3 died. L. pneumophila sg 1 together with several other Legionellae were isolated from the hot water supply to 17 of 20 hospital wards, probably being spread by aerosolization via shower nozzles. Raising the hospital's hot water temperature from 45 degrees C to 65 degrees C, together with heat disinfection of the shower equipment, arrested the outbreak within a week. Keeping the hot water temperature > or = 60 degrees C without chlorination eliminated L. pneumophila from > 75% of the wards. During a period of 2 years after the outbreak we have diagnosed only 1 case of nosocomial legionellosis at the hospital despite an active surveillance program.
A 16-year old boy with an early history of recurrent lower respiratory tract infections exhibited symptoms of prolonged septic fever and liver abscess. Cultures from liver puncture were positive for Staphylococcus aureus, and the patient initially responded to antibacterial therapy. After a period of 4 months, however, the infection relapsed, and further treatment with broad antibacterial, antifungal and tuberculostatic drugs was ineffective. Neither soluble nor particulate stimuli were found to elicit the respiratory burst response in granulocytes from the patient. Spectral analysis of granulocyte cytochrome-b confirmed the diagnosis of chronic granulomatous disease. Since the patient's physical condition deteriorated severely during the prolonged (10-week) septic course, immunosupportive interferon-gamma was added to the anti-microbial therapy. With this regime, the fever subsided and the general condition of the patient improved dramatically. He could be discharged from hospital 9 weeks after the introduction of interferon-gamma and was, at an elective follow-up control 1 month later, convalescing and showed no signs of active infection.
OBJECTIVE: To determine whether the known sequence differences between African and non-African HIV-1 strains are reflected in the serological response. DESIGN AND METHODS: We investigated the antibody reactivity of 34 Swedish, 30 Tanzanian and 42 Zimbabwean HIV-1-positive sera to 67 synthetic peptides with sequences from North American and African HIV-1 isolates, mostly derived from regions of gag and env known to be antigenic. Not all sera were tested against all peptides. RESULTS: Differences in frequency of reactivity were noted with peptides covering the entire third variable domain (V3), which is a primary neutralization determinant, and the carboxyl terminus of gp120, in two regions of gp41, and the carboxyl terminus of p24. In env Tanzanian sera reacted preferentially with a V3 peptide from the strain JY1 (Zaire). Gradual substitutions in the central motif in V3 of ELI from GLGQ to GPGR, typical of many non-African strains, led to a gradual increase in reactivity of many Swedish sera, but did not affect Tanzanian and Zimbabwean sera, suggesting that the major epitopes recognized by these African sera are outside GPGR. V3 peptides from the MN and Z3 strains reacted with most sera, but missed 30% of those of Tanzanian origin. In the carboxyl terminus of gp120 both sets of African sera reacted preferentially with peptides from strains JY1 and MAL. Swedish sera reacted strongest with analogues from strains Z321 and HXB2. In gp41, Swedish sera showed a weak preference for reactivity with HXB2-derived peptides in the immunodominant region (amino acids 590-620), and further towards the carboxyl terminus (amino acids 620-665). CONCLUSION: The differences in serological reactivity were as great between Zimbabwe and Tanzania as between the two African sets and the Swedish. The geographical differences in the pattern of reactivity with HIV peptides probably depend on both host and viral variation and may be developed into a seroepidemiological tool, useful for optimization of future HIV vaccines.
The benefits of antibiotic treatment and a nasopharyngeal culture in children with longstanding cough were analysed in a prospective randomized open study. Clinically suspected pertussis was excluded. Of 40 children given erythromycin for 7 days, 35 (88%) recovered in one week, compared with 17/47 (36%) untreated (p < 0.0001). Erythromycin eliminated Moraxella catarrhalis from the nasopharynx in 21/31 children (68%), compared with spontaneous disappearance in 7/35 (20%) untreated controls (p < 0.001). Purulent bronchitis or otitis media occurred in 2 children (5%) in the treatment group and in 21 (45%) in the control group (p < 0.01). To evaluate the clinical role of isolated pathogens, the 47 untreated subjects were studied. Seven of 35 children harbouring M. catarrhalis recovered, compared with 8/12 in whom this bacterium was absent (p < 0.01). No correlation was found between the isolation of Haemophilus influenzae or Streptococcus pneumoniae and the clinical outcome. Children with persistent cough > 10 days may benefit from erythromycin treatment. M. catarrhalis in the nasopharynx indicates prolonged symptoms and increased risk of bacterial complications.
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The mineral content of the heel bone, and signs of osteoporosis on X-ray of the spine, were evaluated in 26 patients (20 women and 6 men) with giant cell arteritis (GCA), treated with prednisolone for an average period of 5 years. The mean age was 78 years (range 66-95 years). These results were compared with those obtained from a large population study of individuals aged 72, 75, 82 and 85 years. An increase of obvious and severe spinal osteoporosis from 16 to 85% was observed in the women in the population study between the ages of 72 and 85. No additional osteoporosis that could be attributed to the cortisone treatment was found among the GCA patients. The bone mineral content was not reduced in the patients compared to the general population. We conclude that there is no justification for attempting non-steroid treatment in GCA on account of the risk of osteoporosis. Corticosteroids are the only safe treatment for prevention of complications of GCA.
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Immunohistochemical features of infiltrating mononuclear cells (MNC) and resident cells were studied in the temporal artery biopsy specimens of 13 patients with histological verified giant cell arteritis (GCA) and in six biopsy specimens from patients with GCA with negative histological findings. Eight temporal artery biopsy specimens from seven patients with unrelated diseases served as controls. In all patients with GCA proved by biopsy an infiltration of T lymphocytes in the arterial wall was observed, most being of the helper/inducer subset. No B lymphocytes, or very few, were seen. Lymphocytes in 10 out of the 13 positive biopsy specimens displayed staining for the class II major histocompatibility complex (MHC) antigen HLA-DR, whereas this was found in only two of eight controls. A minor number of the infiltrating T lymphocytes from seven out of 13 patients with GCA proved by biopsy stained for transferrin receptors, and in six out of the 13 cases they reacted with anti-interleukin 2 receptor antibody. In the arterial wall from all patients with histologically verified GCA we also found an increased number of macrophages, many of them expressing HLA-DR antigens and transferrin receptors. The immunohistochemical pattern of cell phenotypes found in the arterial wall of patients with GCA suggests that the infiltrating T cells are immunologically activated. This finding supports the hypothesis of a predominantly cellular immunological pathogenesis of giant cell arteritis.
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Ninety patients with giant cell arteritis (GCA) were followed for 9-16 years after diagnosis. Corticosteroids were given to all but one patient. Forty-two patients died during the observation period (27 women and 15 men). The survival was compared with that in the general population and found not to be reduced among the GCA patients. In fact, we found a lower mortality than expected after five years from diagnosis (p less than 0.05). We did not see any increase in deaths due to vascular or malignant diseases in our patients.
The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), fibrinogen and haptoglobin were followed weekly during the initial phase of corticosteroid treatment in 18 patients with 19 episodes of giant cell arteritis (GCA). Fibrinogen and CRP decreased most rapidly, with normal values in 67% of the patients after two weeks of treatment. After two weeks 56% of the patients had normal ESR values and 76% after five weeks. Haptoglobin normalised most slowly, no patient having a normal value after one week, 29% after two weeks and 75% after six weeks. For routine clinical use, we found the ESR alone sufficient for monitoring the initial steroid treatment.
Ninety patients with giant cell arteritis were followed up 9-16 years (median 11.3 years) after diagnosis. The mean duration of corticosteroid therapy was 5.8 years (range 0-12.8 years). Together, the patients had received corticosteroids for 492 patient-years. Five years after diagnosis, 43% of the patients were on corticosteroid therapy. After 9 years, 15 of 60 surviving patients (25%) were still being treated with 1.25-10 mg of prednisolone daily (median dose 5 mg). The relapse rate was about 50%, regardless of the time after diagnosis, when an attempt to withdraw the treatment was made. Forty-six per cent of the relapses occurred within one month and 96% within one year of the end of treatment. Most of the flare-ups occurred during the first year of therapy and in 55% of the patients on a prednisolone dosage of 5 mg or less. We did not find any increase in morbidity in our patients compared to the general population. Nor did we see any significant complications which we could attribute to the steroid treatment.
Two cases of HIV infection associated with Guillain-Barré syndrome are described. The neurologic symptoms started 1 week and 20 weeks, respectively, after the primary HIV infection. Seroconversion for anti-HIV occurred during the disease. A rapid spread of virus to the central nervous system was shown.