Pneumococcal Disease: Invasive Nonvaccine Serotype Emerges

An invasive serotype of Streptococcus pneumoniae (pneumococcus) that belongs to nonvaccine serotype 35B has recently emerged, a recent study has shown.

Sopio Chochua, MD, PhD, from the Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, and colleagues published the results of their study online ahead of print in the June 2017 issue of Emerging Infectious Diseases, CDC’s monthly peer-reviewed public health journal.

“An increase of penicillin-nonsusceptible serotype 35B IPD [invasive pneumococcal disease] and carriage caused by 35B/ST [sequence type] 558 has been apparent in the United States since the introduction of PCV7 [pneumococcal 7-valent conjugate vaccine] in 2000, and it has shown a major increase after PCV13 [pneumococcal 13-valent conjugate vaccine] implementation,” the authors write.

Dr. Chochua and colleagues analyzed data from the CDC’s Active Bacterial Core surveillance (ABCs) program to identify pneumococcal strains that caused IPD in the United States. They used whole-genome sequencing to characterize more than 4,200 pneumococcal strains, including 199 strains of 35B, that caused IPD in 2015 and 2016. They then compared the findings with those from serotype 35B IPD data from previous years.

The PCV7 vaccine covers the seven serotypes of pneumococcus that commonly cause pneumococcal disease in the United States, and first became available in 2000 for infants and children. However, although this vaccine was highly protective against IPD for at least 10 years, emergence of nonvaccine serotypes such as 19A eventually reduced its overall benefit.

Before PCV7 introduction, only 2 different 35B lineages were seen the ABCs program. Although both were relatively rare causes of IPD, they were geographically widespread in the United States, both before and after PCV7 introduction.

According to the investigators, the number of cases of IPD caused by strains of penicillin-nonsusceptible serotype 35B increased after PCV7 was introduced in 2000, and increased even further after PCV13 was introduced ten years later.

“This finding is of concern because even strains that are rarely detected in IPD sometimes rapidly emerge,” the authors note.

They discovered that genetic recombination had resulted in switches in the pneumococcal capsular serotype that produced different 35B variants. One switch involved the 35B/ST558 lineage (the main contributor to antimicrobial-resistant 35B IPD in the post—PCV13 era) and vaccine serotype 9V/ST156. This switch produced strain 35B/ST156, which the investigators identified in six states in 2015 and 2016.

This finding is of concern, they stress, because it demonstrates the significant ability of the ST156 lineage to escape conjugate vaccines. Serotype 19A became the main serotype of the ST156 lineage soon after the introduction of PCV7, and thus, was later included in PCV13. Then 35B serotype emerged as the main serotype of the ST156 lineage after PCV13 was introduced.

Although conjugate vaccines have provided effective and long-lasting protection against IPD, the authors emphasize that continued emergence of serotype 35B and its increasing number of clonal complexes highlights the need for wider-spectrum pneumococcal vaccines.

“Protection against serotype 35B should be considered in next-generation pneumococcal vaccines,” Dr. Chochua and colleagues conclude.

Dr. Parry graduated from the University of Liverpool, England in 1997 and is a board-certified veterinary pathologist. After 13 years working in academia, she founded Midwest Veterinary Pathology, LLC where she now works as a private consultant. She is passionate about veterinary education and serves on the Indiana Veterinary Medical Association’s Continuing Education Committee. She regularly writes continuing education articles for veterinary organizations and journals, and has also served on the American College of Veterinary Pathologists’ Examination Committee and Education Committee.