They describe two cases of toxic shock syndrome (TSS) in children after playing football in new boots. Both developed friction blisters over their Achilles tendons. The blisters contained Staphylococcus aureus, which in one case was found to express the toxic shock syndrome gene (TSS1).

In the first case, a 13-year-old girl developed friction blisters over both heels after playing a competitive game of football in new boots. She was admitted to her local hospital after developing a range of symptoms including fever, rash, abnormally low blood pressure (hypotension), vomiting and diarrhoea.

Further examination revealed a blister, 2cm in diameter, over each of her Achilles tendons containing the bacterium Staphylococcus aureus with the toxic shock syndrome gene (TSS1). A diagnosis of toxic shock syndrome was made and she was treated with antibiotics.

In the second case, a healthy 11-year-old boy played football in a new pair of boots, causing a blister on his right heel. Over the next two days he developed fever, vomiting and diarrhoea, and a rash.

Within hours of admission to hospital, his condition deteriorated and his blood pressure fell. Again, pus from the blister on his heel contained Staphylococcus aureus. He also developed a secondary rash during convalescence.

Toxic shock syndrome has become less common since the link with tampon use was recognised in the 1980s, write the authors. And in children, for whom this association does not apply, the syndrome is rare. But these cases show that the syndrome may follow relatively trivial skin trauma.

They suggest that doctors consider toxic shock syndrome in a child with rash, fever and hypotension. They also stress the need to search carefully for the primary infection, as it may not be immediately obvious, and to be aware that secondary rashes occur.

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"In this network are spots where many proteins interact," she said. "These are key proteins."

These proteins, she said, could be extremely important in insuring normal neuronal function.

"When you step back, you realize this is applicable to any human disease," she said. "You start with a handful of genes you know cause disease and then go find their partners, and then their partners and then build a network that will include all the factors that make you susceptible to a disease or cause the symptoms of it."

"Instead of thinking one gene-one disease, you realize that if there are 10 genes that cause the same symptoms, they must do it through some common pathways or interactions with other proteins."

In applying the network theory to understanding disease, Zoghbi and her colleagues have come full circle. Symptoms used to always be the basis for medical treatment.

"Now we are providing a mechanistic basis for understanding why we treat symptoms," she said.

In the future, treatments may be designed to interrupt the cellular missteps that lead to disease.

Others who participated in this research include: Drs. Chad Shaw, Akash J. Patel and Joseph Fisk, of BCM, Drs. Gabor Szabs, Jean-Frangois Rual, Tong Hao, Ning Li, Alex Smolyar, David E. Hill and Albert-Laszls Barabasi of Harvard. (Drs. Barabasi and Szabs are now at the University of Notre Dame.)

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