Scientists have mapped the genome of a bacterium responsible for the heart-damaging illness known as acute rheumatic fever. In the process, they’ve identified telling genetic differences–many of them introduced by viruses–that distinguish the dangerous pathogen from its less virulent relatives.
People who suffer from rheumatic fever sometimes develop rheumatic heart disease, which causes about 3,600 deaths in the United States each year. Epidemics of the fever hit Salt Lake City in 1986–1987 and 1998–1999 (SN: 11/28/98, p. 346).
The offending bacteria belong to the group A streptococci. Why some infections by these bacteria cause only strep throat while others cause more severe conditions–including rheumatic fever and the flesh-destroying disease known as necrotizing fasciitus–isn’t clear, but certain subtypes of the group are more likely than others to trigger the fever.
Led by James M. Musser of the National Institute of Allergy and Infectious Diseases in Hamilton, Mont., researchers from several U.S. institutions sequenced the genome of a rheumatic-fever-causing streptococcus that belongs to a group A subtype known as M18.
The researchers compared the sequence of that strain with the previously sequenced genome of a strain of subtype M1. Strains of the M1 type are not normally associated with rheumatic fever.
The two sequenced strains share 1,532 genes, the researchers found. The M18 bacterium also has 178 genetic elements that the M1 microbe lacks, while the latter possesses 112 unique elements of its own.
Viruses that infect bacteria often insert genetic material, but these contributions make up a surprising amount of the variation between M1 and M18 streptococci, says Musser. Many of the virus-related genes unique to the M18 strain produce toxins that could account for its virulence, he says.
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The sequence of the type-M18 genome provides a useful map for investigators who wish to mine for factors underlying Streptococcus virulence, comments infectious disease researcher James B. Dale of the University of Memphis (Tenn.).
Musser’s team also compared genetic characteristics of 36 type-M18 streptococci. These included the strain they’ve fully sequenced and bacteria from both outbreaks of rheumatic fever in Salt Lake City. There’s less variation in the virus-contributed genes among the M18 strains than between those strains and the M1 strain, the researchers report in the April 2 Proceedings of the National Academy of Sciences.
Musser notes that the bacteria behind the two Salt Lake City epidemics are virtually identical, indicating that the second outbreak there essentially recycled the strain that caused the first. This similarity suggests that the strain has achieved a stable evolutionary state and can smolder at a low frequency in some populations until unknown factors trigger an outbreak, he says.