New type of pneumococcal infection dominates in wake of vaccine
HOUSTON -- (February 22, 2010) -- The pneumococcal vaccine for infants and children introduced in 2000 caused a precipitous drop in infections until 2005, when serious illnesses began to rise again, especially infections caused by a strain of the pneumococcal bacteria called 19A, said researchers from Baylor College of Medicine and Texas Children's Hospital in a report in the current issue of the journal Pediatrics.
"Of the serotypes (or variants) of Streptococcus pneumoniae (the bacteria that cause pneumococcal disease) now causing invasive disease, 19A is responsible for almost half the infections in children," said Dr. Sheldon Kaplan, head of the section of pediatric infectious diseases at BCM and chief of infectious disease services at Texas Children's. Resistance to multiple common antibiotics occurs in about a third of the serotype 19A isolates, making treatment more difficult.
More protection
The current vaccine called 7-valent pneumococcal conjugate vaccine provides protection against seven strains of the bacteria that until 2000 caused most of the serious disease in children. A new vaccine still under consideration by the U.S. Food and Drug Administration provides protection against 13 types, including 19A.
Pneumococcal disease is a serious illness that results in 5,000 deaths in the United States each year. Most of those who die are age 65 or older, but the bacteria is also the most common cause of invasive or serious disease in children under the age of 2 years. Streptococcus pneumoniae can cause pneumonia, meningitis and an overwhelming blood infection called bacteremia.
The type of pneumococcal vaccine given to older people will not activate the immune system of infants and toddlers to protect them against the disease. The 7-valent vaccine now in use, as well as the proposed 13-valent vaccine, adds a protein to the polysaccharide (sugar) capsule that is similar to that of the bacteria. The polysaccharide capsule is found on the surface of the different forms of the bacteria. The addition of the protein activates the immune system to produce antibodies against the different serotypes of the bacteria.
Keeping track
Kaplan and his colleagues have been keeping statistics on all invasive pneumococcal infections in infants and children at eight U.S. children's hospitals for the past 17 years. He has watched the waning and waxing of pneumococcal infections since the beginning of this century, noting the increase in those caused by 19A.
Infants receive the vaccine at ages 2, 4, and 6 months and a booster between the ages of 12 and 18 months. The vaccine appears to have been efficient in protecting those who received it.
Not only that, but it reduced the infections in parents and grandparents of the children who were vaccinated, he said.
"If you eliminate the organism in the noses of the children, they can't pass it on to the adults," he said.
In 2005, pneumococcal infections began to rise again, he said, but only to about 33 percent above the lowest point in 2004. He and his colleagues found that 19A is responsible for almost half of these infections.
Eye on all 91 strains
Kaplan hopes that approval of the new vaccine comes soon. He said the Centers for Disease Control and Prevention and the American Academy of Pediatrics are already designing a "catch-up" strategy to protect youngsters who have received the old vaccine in the meantime.
"There is nothing to prevent another type of pneumococcal serotype from arising," he said. "So far, the other strains don't seem to have that potential to the same degree as 19A."
"A goal is to develop a vaccine with proteins common to all 91 strains that would lead to an antibody that is protective against all the serotypes. No one anticipates that will happen soon."
Others who took part in this study include Drs. William J. Barson of Ohio State University College of Medicine and Public Health in Columbus; Philana L. Lin of the University of Pittsburgh Medical Center; Stephanie H. Stovall of the University of Arkansas for Medical Sciences in Little Rock; John S. Bradley of Rady Children's Hospital San Diego; Tina Q. Tan of Northwestern University Medical School in Chicago; Jill A. Hoffman of the University of Southern California School of Medicine in Los Angeles; Laurence B. Givner of Wake Forest University School of Medicine in Winston-Salem, N.C.; and Edward O. Mason Jr. of BCM.
Funding in part for this work came from Pfizer/Wyeth Pharmaceuticals.
For more information on research at Baylor College of Medicine, please go to www.bcm.edu/fromthelab and www.bcm.edu/findings.