Two outbreaks of trichinosis occurred in France in August and October of 1985 and 1,073 cases in all were identified. In the first outbreak, two localities were involved: the town of Melun and the 14th district of Paris. To determine the origin of the contamination, three case-control studies were carried out: among patients' families, among the populations of these two areas, and among the inmates in the prison of Melun. In the second outbreak, cases again occurred in Paris but in a different district (the 12th), in the city's suburbs, and in other towns scattered throughout France. Although no parasites were found in any of the meat examined in either outbreak, results of the study indicate that infection was due to horsemeat consumption and led to the incrimination of two carcasses, one imported from a slaughterhouse in the United States and the other from West Germany. These findings led the French Ministry of Agriculture to order the inspection for trichinosis of all meat from horses slaughtered both in France and in countries exporting horsemeat to France.

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The clinical features, brain computerized tomography (CT) scans and cardiological findings of nine patients with neurotrichinosis are reviewed. Neurological signs consisted of encephalopathy and focal deficits with small hypodensities in the cortex and white matter, detected by the CT scans. Various cardiovascular events were also observed in eight out of nine patients. They were usually concomitant with neurological symptoms and mainly consisted of myocardial injury as assessed by electrocardiographic and plasma creatine phosphokinase (CPK)-MB isoenzyme changes. The cardio-neurological syndrome developed early in the course of the disease at a time of marked hypereosinophilia and the percentage of patients with eosinophilia > or = 4000 mm3 was significantly higher in the patients with neurological dysfunction than in those without neurological signs. We selected the following criteria to describe the distinctive cardio-neurological syndrome related to trichinosis: (i) early onset of neurological symptoms (within a few days) after the first general symptoms; (ii) central nervous system involvement consisting of both diffuse encephalopathy and focal neurological deficits, usually of simultaneous onset; (iii) concomitant acute myocardial injury and/or infarction; (iv) marked hypereosinophilia (> or = 4000/mm3) at time of first cardio-neurological events; (v) brain CT scan showing small hypodensities in the hemispheric white matter or cortex. Post-mortem examination of one patient revealed ischaemic lesions with multiple arteriolar microthrombi in the brain and myocardium. This was consistent with the brain CT scan and electrocardiographic data and suggested that neurotrichinosis is an expression of a multi-organ disorder associated with hypereosinophilia, that is characterized in most patients by simultaneous neurological and myocardial manifestations basically related to ischaemia.

To determine the therapeutic usefulness of benzimidazoles in trichinellosis, 117 patients from a single outbreak were treated either with albendazole alone (N = 59) or with a regimen including tiabendazole followed by flubendazole (N = 58). The criteria of disease activity were evaluated at days 1, 7, 15, and 45. No difference was found between the two groups with regard to the evolution of myalgia, fever, fatigue, new clinical manifestations, or laboratory and serologic data. Both treatment regimens were well tolerated. In all, 30 patients of the albendazole group and 29 of the tiabendazole-flubendazole group were reevaluated 16 months later. Serology was negative in 70% of the albendazole-treated patients vs 34.5% of the tiabendazole-flubendazole-treated patients (P less than 0.01). The muscle biopsy examination of nine patients suggested less parasitic infection in the albendazole group. In conclusion, no difference was noted during the early therapeutic responses to the drugs used, but albendazole might be more effective than the other regimen in treating residual larval infestation estimated 16 months after the onset of the disease.

Fenoverine is a spasmolytic drug that inhibits calcium channel currents. We describe the clinicopathologic find ings in two patients with fenoverine-induced rhabdomyo lysis, of whom one died. A transient left-bundle-branch block was observed in both patients. In one case, pre-exist ing hepatic dysfunction may have induced accumulation of the drug. Concurrent treatment by fibrates, as observed in the second patient, may have been a predisposing factor for fenoverine-induced rhabdomyolysis. The incidence of muscular complications of fenoverine therapy could be reduced by avoidance of prescription of the drug in patients with hepatopathy or those being treated with cho lesterol-lowering agents. Physicians should be aware of life-threatening adverse effects of apparently innocuous drugs.