Little is known about the etiology of adenocarcinoma of the distal esophagus/cardia, a cancer which has increased in incidence in the United States over the last two decades. We analyzed data on smoking, alcohol use, dietary intake, and other factors obtained from 173 hospitalized males with adenocarcinoma of the distal esophagus/cardia (cases) and 4,544 hospitalized males with diseases not related to smoking and of other organ systems than the gastrointestinal tract (controls). Cases of squamous cell carcinoma of the esophagus (n = 136) and adenocarcinoma of the distal stomach (n = 122) were included as separate case groups. All subjects were interviewed in 28 hospitals in eight cities in the US between 1981 and 1990. After adjustment for covariates, the odds ratio (OR) for adenocarcinoma of the distal esophagus/cardia for current smokers was 2.3 (95 percent confidence interval [CI] = 1.4-3.9) and that for ex-smokers was 1.9 (CI = 1.2-3.0) relative to never-smokers. The OR for drinkers of four or more ounces of whiskey-equivalents of alcohol per day (relative to those consuming less than one drink per week) was 2.3 (CI = 1.3-4.3). Intakes of total fat and vitamin A from animal sources were significant risk factors and fiber intake was associated inversely with adenocarcinoma of the distal esophagus/cardia. Although the number of female cases of adenocarcinoma of the distal esophagus/cardia was small (n = 21), significant associations were observed for smoking and alcohol.

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A mass outbreak of severe acute respiratory syndrome (SARS) in the Amoy Gardens housing complex in Hong Kong at the end of March, 2003, affected more than 300 residents in less than a month, and has epidemiologists all over the world puzzled about the mode of transmission of this new disease, which until then was thought to be transmitted solely by respiratory droplets. The source of the outbreak was later traced to an individual with SARS who spent two nights at Amoy Gardens. Official explanations failed to account for the large number of residents infected over a wide area within a short time. A powerful environmental mechanism that efficiently amplified and distributed the causal agent must have been at work to cause this outbreak. One such mechanism could be an animal vector, most probably roof rats, that was infected by the index patient and subsequently spread the disease to more than 150 households.

A strain of Veillonella parvula M4, which grows readily in lactate broth without a requirement for carbon dioxide, has been isolated from the oral cavity. Anaerobic, washed cells of this organism fermented sodium lactate to the following products (moles/ 100 moles of lactate): propionate, 66; acetate, 40; carbon dioxide, 40; and hydrogen, 14. Cells grew readily in tryptone-yeast extract broth with pyruvate, oxaloacetate, malate, and fumarate, but poorly with succinate. The fermentation of pyruvate, oxaloacetate, or lactate plus oxaloacetate by washed cells resulted in the formation of propionate and acetate in ratios significantly lower than those observed with lactate as the sole carbon source. This was primarily due to increased acetate production. Cell-free extracts were unable to degrade lactate but metabolized lactate in the presence of oxaloacetate, indicating the presence of malic-lactic transhydrogenase in this organism. Lactic dehydrogenase activity was not observed. Evidence is presented for oxaloacetate decarboxylase and malic dehydrogenase activities in extracts.

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