[An investigation of a food poisoning incident caused by Amanita fuliginea].

Mistakenly picking and eating poisonous mushrooms can cause acute poisoning. In August 2020, Qingdao Hospital of Traditional Chinese Medicine handled a poisonous mushroom poisoning incident, conducted epidemiological investigation on all poisoned patients, collected suspicious food, clinical manifestations, clinical test results and treatment conditions, and identified the mushrooms as Amanita fuliginea poisoning after morphological identification. In this incident, 6 people ate grey goose paste, of which 4 were sick with a incubation period of 6~12 h. The clinical manifestations were gastrointestinal symptoms such as nausea, vomiting and diarrhea, liver and kidney damage. After symptomatic support treatment, hemoperfusion or continuous hemofiltration treatment, the patients were cured and discharged. It is suggested to strengthen the popular science education on poisonous mushroom poisoning and improve the ability of identification and clinical treatment of poisonous mushrooms in grass-roots medical institutions.

Spontaneous bacterial empyema caused by Aeromonas veronii biotype sobria.

Spontaneous bacterial empyema is a complication of hepatic hydrothorax in cirrhotic patients. The pathogen, clinical course and treatment strategy are different to the empyema secondary to pneumonia. A 54-year-old man, who was a cirrhotic patient with hepatic hydrothorax, was admitted to National Taiwan University Hospital for fever, dyspnea and right side pleuritic pain. The image study revealed massive right pleural effusion and no evidence of pneumonia. The culture of pleural effusion yielded Aeromonas veronii biotype sobria. The diagnosis of spontaneous bacterial empyema caused by Aeromonas veronii biotype sobria was established. To our best knowledge, Aeromonas veronii biotype sobria had never been reported in English literature as the causative pathogen of spontaneous bacterial empyema.

Imported malaria: successful treatment of 31 patients in the era of chloroquine resistance.

The diagnosis and management of imported malaria presents a continuing challenge in developed countries, including Taiwan. We retrospectively analyzed the records of all 31 patients with imported malaria treated at National Taiwan University Hospital from January 1984 through December 1998. Plasmodium falciparum was identified as the causative malarial parasite in 18 patients, P. vivax in 12, and P. ovale in one. All 31 patients had fever, but only 13 presented with the characteristic fever pattern. The most common initial laboratory abnormalities were thrombocytopenia (20/31), mild hyperbilirubinemia (20/31), and leukopenia (7/31). The median time from the onset of fever to the correct diagnosis was 4 days for P. falciparum and 5 days for P. vivax. In 28 cases, the clue that led to early diagnosis was the patient's travel history. Quinine, but not chloroquine, was effective in 17 out of 18 cases of falciparum malaria. Three patients treated with intravenous quinine required a change of regimen because of life-threatening quinine toxicity; artesunate served as a safe and effective alternative in this situation. While most patients with tertian malaria were cured with the standard chloroquine and primaquine regimen, a higher dosage was required for one case acquired in Papua New Guinea. All patients, including two with severe malaria, survived. We conclude that, the mortality of imported malaria in the chloroquine resistance era can be minimized with early recognition by obtaining a thorough travel history, and instituting appropriate antimalarial chemotherapy based on precise identification of species. Quinine toxicity should be closely monitoried, especially when this drug is given intravenously.

Antibodies to hepatitis C virus in autologous blood donors.

Hepatitis C virus (HCV) is the major cause of posttransfusion hepatitis. Two anti-HCV enzyme immunoassay (EIA) kits and one recombinant immunoblot assay (RIBA) were used to test serum samples of 1476 donations from 692 autologous blood donors to assess the prevalence of anti-HCV and its relationship to transfusion history. Of all autologous blood donations, 23 (1.6%) reacted when tested with one EIA kit and 29 (2.0%) reacted when tested by the other EIA kit. Of the autologous donors, 12 (1.78%) reacted by the first EIA kit and 14 (2.02%) by the second. Discrepancies in the EIA results from different donations by the same donor were seen in seven donors. The RIBA was positive or indeterminate in 33 percent of the EIA-reactive donations and in 41 percent of EIA-reactive donors. All RIBA-positive and -indeterminate samples reacted with both EIA kits. There was no significant difference in the EIA-reactive rates of autologous and first-time homologous blood donors. Previously transfused autologous blood donors had a higher anti-HCV EIA-reactive rate than nontransfused autologous donors, but the difference was not significant. In regard to hepatitis C, the use of autologous blood for homologous transfusion appears to be as safe as the use of blood from first-time homologous donors. Universal testing of previously transfused patients for hepatitis C appears premature at this time. Discrepant anti-HCV EIA results from different donations from the same individual have implications regarding donor deferral.