Botulism commonly occurs when the anaerobic, gram-positive bacterium Clostridium botulinum, under suitable conditions, produces botulinum neurotoxins. Named A-F, these toxins are the immediate causative agent of the clinical symptoms of symmetrical, descending neurological deficits, including respiratory muscle paralysis. We present five cases of foodborne botulism occurring in Greenland, two with fatal outcome, caused by ingestion of tradionally preserved eider fowl. In the cases of the survivors, antitoxin and supportive care, including mechanical ventilation, were administered. In these cases recovery was complete. Microbiological assays, including toxin neutralization bioassay, demonstrated the presence of neurotoxin E in two survivors. The third survivor was shown by PCR to have the BoNT type E gene in faeces. This is the first report of cases of fatal botulism in Greenland. It underscores the importance of prompt coordinated case management effort in a geographically isolated area such as Greenland.
A 65-year-old woman developed severe chorea as the presenting symptom of the hyperviscosity syndrome together with polycythemia vera and an ovarian cyst. Whole blood viscosity was 69.5 centipoise at a shear rate of 1.1 s-1 (normal 12.0-22.0 centipoise). After four phlebotomies the chorea subsided completely, and the blood viscosity became normal. Hemoglobin level was stable at normal range and then increased to 18.0 g/dl with recurrence of the faciobuccal dyskinesia that disappeared promptly following the phlebotomies. This case emphasizes that in elderly patients with neurological disorders, such as chorea, polycythemia should be strongly considered as one of the treatable causes.
Introduction. Contrary to a widely held belief, ischaemic cerebral infarction is not a rare disease in Greenland, as shown recently by our institution. We report data on some of the known risk factors in patients below 60 years of age with ischaemic stroke. Method. Retrospective data collection and review of charts from Greenlandic patients from all of Greenland admitted to the central hospital, Dronning Ingrids Hospital in Nuuk, in the years 2001 and 2002. Results. A total of 37 patients below 60 years of age were discharged with a diagnosis of cerebral infarction. All had a CT, which showed infarction in 32. Five were reported normal, and the diagnosis of infarction rested on the absence of haemorrhage combined with long-standing, major neurological defect. Median age of the group was 54 years. Fifteen (40%) were women, thirty (81%) were smokers. Nine (24%) had hypertension. Two had diabetes, one had atrial fibrillation, and one had dilated cardiomyopathy. Two had significant carotid atherosclerosis diagnosed by duplex ultrasound. Of the rest, fifteen had transoesophageal echocardiography done, thirteen of which showed atherosclerotic changes. The cholesterol levels showed relatively high HDL levels. Conclusion. Ischaemic stroke is a common disease in young Greenlanders and seems to be associated with atherosclerosis with smoking as the only outstanding risk factor -though not more common than in the general population.
A middle-aged patient of Greenlandic origin was referred for skin infection of the leg. An initial minor trauma of the skin of the distal right lower extremity was complicated by bullous erysipelas which cultured positive for group A β-hemolytic streptococci (GABHS). The clinical condition deteriorated and necrotizing fasciitis developed despite relevant surgical and antibiotic treatment. Approximately 3 weeks later, the patient developed arthralgia, impaired renal function with azotemia, hypertension and severe nephrotic syndrome with periorbital and peripheral edema. A kidney biopsy demonstrated endocapillary glomerulonephritis. Concomitantly, carditis with chest pain, moderately reduced left ventricular ejection fraction and mitral regurgitation were noted. The patient had no signs of pharyngitis in the whole period. The patient thus contracted poststreptococ glomerulonephritis and furthermore she fulfilled the criteria of acute rheumatic fever following a GABHS skin infection. We suggest a possible relation between a virulent GABHS clone causing NF and ARF
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