Abstract

In 1907, when the first case of Whipple disease was described by George Whipple, the clinical presentation of the disease, although not considered to be of infectious origin, already included cough and diarrhea [1]. This index patient had a chronic form of the disease, coined here as lateonset Whipple disease. During the past century, Whipple disease has been considered to be a rare and chronic disease, mainly affecting white, middle-aged men and presenting mainly as diarrhea, weight loss, steatorrhea, arthralgia, lymphadenopathy, anemia, and, to a lesser extent, neurologic impairments, ocular involvement, and/or endocarditis [2]. The visualization by electron microscopy of rods in intestinal biopsy specimens suggested that Whipple disease was of microbial origin [3, 4], a hypothesis confirmed in the 1990s by sequencing the 16S ribosomal RNA encoding gene of the causative bacteria [5, 6], named Tropheryma whipplei [7]. However, our understanding of the ep-

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