Antibiotics are medicines used to kill the bacteria that cause disease. However, bacteria can change—or mutate—making it possible to resist antibiotics. This is known as antibiotic resistance. Many bacteria, including Streptococcus pneumoniae (pneumococcus), have become resistant to one or many antibiotics. Resistance can lead to treatment failures.
Until 2000, pneumococcal infections caused 60,000 cases of invasive disease each year. Up to 40% of these infections were caused by pneumococcal bacteria that were resistant to at least one antibiotic. These numbers have decreased greatly following:
- The introduction of pneumococcal conjugate vaccines for children
- A change in definition of non-susceptibility (resistance) to penicillin in 2008
In 2011, there were about 37,000 cases of invasive pneumococcal disease. Available data show that pneumococcal bacteria are resistant to one or more antibiotics in 31% of cases. How common drug-resistant Streptococcus pneumoniae (DRSP) is depends on what part of the country you live in.
There are more than 90 strains (serotypes) of pneumococcus bacteria. Seven serotypes (6A, 6B, 9V, 14, 19A, 19F, and 23F) accounted for most DRSP before the introduction of the 7-valent pneumococcal conjugate vaccine (PCV7, Prevnar®) in the United States in 2000. Most antibiotic resistance today is found in serotype 19A, which is included in the newer 13-valent pneumococcal conjugate vaccine (PCV13, Prevnar 13®) introduced in the United States in February 2010.
PCV7 prevented many infections due to drug-resistant pneumococci, and it is expected that the 13-valent vaccine will prevent additional infections caused by drug-resistant pneumococcal strains.
Outbreaks of DRSP have been reported in nursing homes, institutions for HIV-infected persons, and child-care centers.
DRSP is associated with increased costs compared to infections caused by non-resistant (susceptible) pneumococcus. This is because of the need for more expensive antibiotics; repeat disease due to treatment failures; the need for surveillance to track resistance patterns; educational requirements for patients, physicians, and microbiologists; and new antibiotic drug development.
If you attend or work at child-care centers, you are at increased risk for infection with DRSP. Among those with pneumococcal infections, those who recently used antibiotics are more likely to have a resistant infection than those who have not.
CDC sponsors the Active Bacteria Core surveillance (ABCs), an active, population-based surveillance system in 10 states. In addition, all types of invasive pneumococcal disease (including DRSP) are included in the national public health surveillance system. Several private-sector systems also track DRSP.
Prevention: Challenges and Opportunities
There are several challenges for preventing emerging resistance of pneumococcus, including:
- Widespread overuse of antibiotics
- Spread of resistant strains
- Underuse of the 23-valent pneumococcal polysaccharide vaccine (PPSV23) recommended for adults and high-risk children
- Lack of adoption by some clinical laboratories of standard methods (NCCLS guidelines) for identifying and defining DRSP
- Lack of vaccine availability to protect against all strains of pneumococcus
Campaigns for more judicious use of antibiotics and expanded use of vaccines may slow or reverse emerging drug resistance. Prevention of infections could improve through expanded use of PPSV23 and PCV13. Of note, among children 5 years of age or younger, PCV13 includes serotypes associated with about 80% of invasive pneumococcal isolates that are resistant to penicillin.
- Active Bacterial Core surveillance, 1996-2000.
- Clinical and Laboratory Standards Institute. Performance standards for antimicrobial susceptibility testing; eighteenth informational supplement. CLSI document M100-S18. Wayne, PA: Clinical and Laboratory Standards Institute; 2008.
- Active Bacterial Core surveillance, 2011.
- Hampton LM, Farley MM, Schaffner W, et al. Prevention of antibiotic-nonsusceptible Streptococcus pneumonia with conjugate vaccines. J Infect Dis 2012;205:401-411.
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