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Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems. 
Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems.
Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems.