Sunday, January 08, 2006

Goodpasture syndrome and Spanish Flu

There is an under appreciated historical connection between Goodpasture syndrome and the 1918 pandemic (Spanish) flu. We are traditionally taught that Goodpasture syndrome is a pulmonary-renal syndrome characterized by pulmonary hemorrhage and rapidly progressive glomerulonephritis due to antiglomerular basement membrane (anti-GBM) antibodies. But “Goodpasture syndrome” is a misnomer. The patient with pulmonary and renal disease described by Ernest Goodpasture in 1919 (Goodpasture EW. The significance of certain pulmonary lesions in relation to the etiology of influenza. Am J Med Sci 1919;158:863-70) was presented as a case of influenza and probably did not have anti-GBM disease. Yet the myth of Goodpasture syndrome persists. It was a particularly unfortunate misattribution because it diverted attention from Goodpasture’s most monumental work at Vanderbilt in 1931, the development of a chick embryo technique for viral culture. Although this ground breaking work spurred a revolution in virology and brought fame to the Pathology department at Vanderbilt, [1] over time it tended to be forgotten, being overshadowed by the eponymic association with anti-GBM disease.

The story of Ernest Goodpasture, pandemic influenza and anti-GBM disease is controversial and seems to vary with every telling. Perhaps the most reliable account can be found in the biography by Robert D. Collins, “Ernest William Goodpasture—Scientist, Scholar, Gentleman.” On pp. 64-67 we find Goodpasture in the Navy Medical Corps in 1918-19, stationed at the Chelsea Naval Hospital near Boston. There he was responsible for performing autopsies of victims of the influenza pandemic. Because many patients with the disease developed secondary bacterial pneumonia it was widely believed that influenza had a bacterial etiology. But Goodpasture postulated a viral etiology and believed that the primary etiologic agent could cause pneumonia. Therefore he was interested in finding cases of influenza pneumonia with negative bacterial cultures. Two such cases formed the basis of his 1919 paper. One of the two was described as unusual in that while the pulmonary pathologic findings were consistent with influenza the pulmonary hemorrhage was profuse and glomerular inflammation was found. It is unclear what underlying disease other than influenza this patient may have had. Attempts to retrieve the slides from Chelsea years later for further study were unsuccessful. According to Collins, Goodpasture did not approve of the association of his name with this syndrome. He writes “In this case, good intentions---recognizing Dr. Goodpasture---paved the road to inaccuracy and inappropriateness.”

And so, with apologies to Paul Harvey: Now you know the rest of the story.

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