Researchers have a new theory to explain why a particularly nasty strain of Salmonella has spread through U.S. and European poultry populations in the past 40 years, sickening millions of people who eat the infected birds or their eggs. Efforts to quell two Salmonella strains dangerous to chickens but harmless to humans, they say, inadvertently unleashed the strain plaguing us today.
Cases of serious food poisoning linked to Salmonella enteritidis have increased steadily since the 1960s. Tens of thousands of people are hospitalized and hundreds are killed yearly by this strain in the U.S. alone; most cases result from eating undercooked eggs or chicken. No one knew why S. enteritidis has come on so strong--illness from another strain also found in poultry, Salmonella typhimurium, has held steady over the same period. Meanwhile, Salmonella gallinarum and Salmonella pullorum--both of which sicken chickens but not humans--have been largely eradicated from chickens in the developed world thanks to simple tests that allow farmers to cull infected flocks.
Now a team led by microbiologist Andreas Bäumler of Texas A&M University in College Station suggests that these culling programs have allowed S. enteritidis to thrive. It, S. gallinarum, and S. pullorum are all coated with long sugar chains that make them indistinguishable to the chicken immune system, the researchers say. Earlier in the century, flocks were frequently exposed to the chicken pathogens, which spurred their immune systems to fight all three strains. But with the chicken pathogens beaten back, levels of the antibodies that fight all three strains have fallen in the birds, allowing S. enteritidis, which elicits little or no immune response, a greater foothold, the researchers suggest in the 7 January issue of Science. The theory is supported by epidemiological data, says Baümler, which show that S. enteritidis infections in people increased steadily as other Salmonella strains were eradicated from chickens. And the sugar coat of S. typhimurium is different from that of the other strains, which could explain why it hasn't boomed.
"It's a very ingenious and pretty simple hypothesis," says bacterial geneticist Ferric Fang of the University of Colorado Health Sciences Center in Denver. "Unwittingly, people improved life for chickens but harmed human health," he says. Bäumler says that if his team's scenario is true, it suggests a new method for fighting S. enteritidis, which is difficult to detect: immunize chickens against one of the related strains with existing vaccines, and the birds may also be able to ward off infections that endanger humans.
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