BOSTON — Community-acquired methicillin-sensitive
Staphylococcus aureus caused 65% of invasive infections in children at
Texas Children’s Hospital in 2010, according to a study presented here at
the IDSA 49th Annual Meeting.
CA-MSSA has steadily increased as a cause of these
infections in children, according to Kristina G. Hulten, PhD, and
colleagues from Baylor College of Medicine and Texas Children’s Hospital
“Things are changing,” Hulten said. “In
the past few years, we have begun to see a shift and we are seeing more CA-MSSA
infections in children.”
Nearly 60% of invasive community-acquired S. aureus
infections were caused by methicillin-resistant S. aureus (MRSA)
(>90% USA300), at Texas Children's between 2001 and 2006. During this same
time, a steady increase of invasive CA-MSSA infections was noted, 25% of which
were caused by USA300. Most invasive CA-MSSA USA300 isolates (25/29, 86%) were
Panton-Valentine leukocidin (PVL)-positive, while only 12% (10/86) of invasive
non-USA300 CA-MSSA isolates carried PVL, according to the study results.
Hulten said that the increasing presence of PVL in
non-USA300 MSSA isolates suggests an advantage of these genes for the organism
and may, in part, explain the rise in invasive CA-MSSA infections at Texas
Infectious Diseases in Children Editorial
Board Member Sheldon L. Kaplan, MD, who is a co-author of the study,
said that this phenomenon is mostly unexplainable.
“From 2000 to 2005, MRSA was more common than MSSA
as an invasive isolate in community-acquired infections, but now the reverse is
true and we are seeing increasing numbers of susceptible isolates and a decline
in methicillin-resistant isolates,” Kaplan said. “These isolates are
non-USA300 background, so it seems as if the PVL genes are becoming more common
among MSSA isolates. And all of the community MRSA isolates are PVL positive
even though it used to be only about 5%.”
The investigators identified invasive CA-MSSA isolates
from 2007 to 2010 from the hospital’s S. aureus surveillance
database. The isolates were analyzed by PFGE and by PCR for the PVL genes and
arcA (ACME cassette gene).
A total of 179 children with invasive CA-MSSA infections
were identified, and 150 (84%) isolates were available for study. Overall,
CA-MSSA represented 179/352 (51%) of the total invasive community-acquired
S. aureus infections and the proportion of invasive isolates being MSSA
increased yearly from 39% in 2007 to 52% in 2009 (P<.001).
Of 150 analyzed isolates, 42 were USA300 and related
isolates and 108 were of other PFGE patterns. The USA300 and related isolates
decreased from 11/29 (34%) isolates in 2007 to 9/45 (13%) in 2010
(P=.03). By PCR, 92/150 (61%) isolates were PVL positive, and none of
the isolates carried the arcA gene.
Of the USA300 isolates, 26 (62%) were resistant to
erythromycin and three (7%) were resistant to clindamycin. Of non-USA300
isolates 23 (21%) were resistant to erythromycin and 14 (13%) were resistant to
The mean age of the patients was 7.6 years and 62% were
male. Invasive infections included osteomyelitis (n=98), septic arthritis
(n=22), pneumonia/empyema (n=13), myositis/pyomyositis (n=10), bacteremia
(n=4), lung/ retropharyngeal abscess (n=2) and cellulitis with bacteremia
Further investigation is warranted to explain the causes
of the increase of CA-MSSA invasive infections. — by Cassandra A. Richards
Disclosures: Dr. Hulten reports no relevant financial
disclosures. Dr. Kaplan reports receiving research funding from Pfizer.
For more information:
- Hulten K. #1164. Presented at: IDSA 49th Annual
Meeting. Oct. 20-23, 2011. Boston.