Issue: October 2005
October 01, 2005
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Increased nasal colonization of MRSA in children noted

Nasal carriage of S. aureus is a significant factor in developing infection; more than 80% of isolates that cause infection originate in the nose.

Issue: October 2005
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Although a 2001 study by Vanderbilt University showed that nasal colonization of methicillin-resistant Staphylococcus aureus (MRSA) in healthy children was infrequent, a follow-up study suggests increasing frequency of MRSA colonization in healthy children.

image
Methicillin-resistant Staphyloccocus aureus (MRSA)
Source: CDC/Janice Carr

The increase in nasal colonization could be a major factor in the increase of community-associated MRSA (CA-MRSA) infections in children, according to researchers from Vanderbilt University Medical Center in Nashville, Tenn.

CDC officials define CA-MRSA infections as those infections that are acquired by people who have not been recently hospitalized or had a medical procedure.

CA-MRSA causes more than 50% of all community-associated S. aureus infections in some areas, the researchers said in the report. Nasal carriage of S. aureus is a significant factor in developing infection; more than 80% of isolates that cause infection originate in the nose.

In the 2001 study, the researchers demonstrated that the nasal carriage rate of MRSA in children in Nashville was 0.8%, consistent with previously published rates ranging from 0.2% to 2.2%. Two other studies that analyzed the MRSA colonization of children in the Chicago area also demonstrated similar rates of MRSA carriage at that time (0.6% to 1.7%).

Increase in S. aureus, MRSA

The follow-up study conducted three years later found that the pediatric carriage rate of MRSA in Nashville to be 9.2%, a tenfold increase since 2001, researchers said.

chart
Methicillin-resistant Staphyloccocus aureus (MRSA)
Source: CDC/Janice Carr

C. Buddy Creech, MD, clinical/research fellow in pediatric infectious diseases at Vanderbilt, and colleagues designed the current study to compare with the previous study: They used the same population group, collection techniques, identification protocols and inclusion and exclusion criteria. And, they collected the samples during the same season of the year. The researchers excluded patients who were experiencing any acute illnesses.

The researchers collected nasal swabs from 500 children aged 2 weeks to 21 years who were seeking health maintenance visits from either Vanderbilt University Medical Center Pediatric Primary Care Clinic (n = 249) or Old Harding Pediatric Associates (n = 251), also in Nashville. They gathered the swabs between April and Sept. 2004. The researchers collected questionnaires in order to obtain medical, family and social histories, as well as demographic data.

The researchers noted that 182 children were colonized with S. aureus. Of these, 84 of the isolates showed growth on selective media and 46 isolates (9.2%) were confirmed to be MRSA by detection of the mecA gene. Creech and colleagues looked for the presence of specific virulence factors, such as the Panton-Valentine Leukocidin, and further analyzed them for antibiotic susceptibility.

Forty-five of the 46 isolates (98%) were susceptible to gentamicin, rifampin and trimethoprim/sulfamethoxazole. Twenty-five of the isolates (54%) were resistant to erythromycin, and 12 (26%) were resistant to clindamycin. The researchers detected inducible clindamycin resistance with a positive D test in eight of the 25 (32%) erythromycin-resistant isolates.

The researchers also noted that nasal carriage of S. aureus increased from 29% in 2001 to 34% in 2004, in addition to the tenfold increase in nasal carriage of MRSA.

This difference seems to be due to the rise in CA-MRSA colonization, though the rates of carriage with methicillin-susceptible S. aureus did not change between the two study periods.

Results not surprising

The researchers anticipated a modest increase (3.2%) in MRSA colonization and enrolled a sufficient number of children to detect such a difference. “We were not surprised to find that colonization had increased, given the frequency in which we are seeing CA-MRSA infections in children and adolescents,” Creech told Infectious Disease News.

CA-MRSA is not a reportable disease, making it difficult to track. However, Creech noted that in 2004, 62% of the positive staphylococcal cultures from children with skin lesions and abscesses in the pediatric emergency department of the Monroe Carell Jr. Children’s Hospital at Vanderbilt were methicillin resistant.

The researchers assessed risk factors associated with CA-MRSA colonization; however, they found no differences based on age, ethnicity, gender or history of antibiotic use. The only association noted was a greater risk of MRSA colonization in children who live with someone who works in a hospital or clinic (OR 2.0, P=0.04). This association was also noted in the 2001 study.

They also obtained family members’ histories pertaining to whether they ever experienced skin lesions or abscesses, but the researchers found no differences between the children that were colonized and those who were not, Creech said.

Further studies in other locations and populations are needed in order to determine the host pathogen determinants of colonization, according to the researchers.

In addition, further studies will help researchers determine strategies to deter MRSA transmission and to develop novel treatments and vaccines. Ongoing studies are underway by this group to understand nasal colonization in a variety of settings, including healthy adults.

In the meantime, CDC officials recommend keeping hands and open wounds clean with soap, water and alcohol-based hand sanitizers.

For more information:
  • Creech CB, Kernodle DS, Alsentzer A, et al. Increasing rates of nasal carriage of methicillin-resistant Staphylococcus aureus in healthy children. Pediatr Infect Dis J. 2005;24:617-621.
  • Nakamura MM, Rohling KL, Shashaty M, et al. Prevalence of methicillin-resistant Staphylococcus aureus nasal carriage in the community pediatric population. Pediatr Infect Dis J. 2002;21:917-922.