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Gerald T. Keusch

Researcher at Boston University

Publications -  327
Citations -  15204

Gerald T. Keusch is an academic researcher from Boston University. The author has contributed to research in topics: Shiga toxin & Toxin. The author has an hindex of 62, co-authored 327 publications receiving 14572 citations. Previous affiliations of Gerald T. Keusch include Boston Medical Center & Christian Medical College & Hospital.

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Journal ArticleDOI

Infection and diabetes: The case for glucose control

TL;DR: Good control of blood sugar in diabetic patients is a desirable goal in the prevention of certain infections (Candida vaginitis, for example) and to ensure maintenance of normal host defense mechanisms that determine resistance and response to infection.
Journal ArticleDOI

Quinolone Antibiotics Induce Shiga Toxin-Encoding Bacteriophages, Toxin Production, and Death in Mice

TL;DR: Treatment of human STEC infection with bacteriophage-inducing antibiotics, such as fluoroquinolones, may have significant adverse clinical consequences and that fluoroquolone antibiotics may enhance the movement of virulence factors in vivo.
Book ChapterDOI

Shiga toxin: biochemistry, genetics, mode of action, and role in pathogenesis.

TL;DR: The definitive description of this organism was provided by Kiyoshi Shiga following an extensive dysentery epidemic in Japan in 1896 (Shiga 1898), and in 1900 Flexner concluded that shigellosis was due to a “toxic agent rather than to an infection per se”.
Journal ArticleDOI

Pathogenesis of shigella diarrhea. XI. Isolation of a shigella toxin-binding glycolipid from rabbit jejunum and HeLa cells and its identification as globotriaosylceramide.

TL;DR: These studies show an identical carbohydrate- specific glycolipid receptor for shigella toxin in gut and in HeLa cells and the possibility that the pilus and toxin B subunit contain homologous sequences.
Journal ArticleDOI

The History of Nutrition: Malnutrition, Infection and Immunity

TL;DR: The cyclical relationship between poor nutrition, increased susceptibility to infectious diseases, leading to immunological dysfunction and metabolic responses that further alter nutritional status is described and, wherever possible, related to physiological mechanisms are described.