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Letter
Panton-Valentine Leukocidin Genes in Staphylococcus
aureus
Damian C. Melles,* Willem B. van Leeuwen,* Hélène A.M.
Boelens,* Justine K. Peeters,* Henri A. Verbrugh,* and Alex van Belkum*
*University Medical Center Rotterdam, Rotterdam, the
Netherlands
Suggested citation for this article
The pathogenicity of Staphylococcus aureus depends on
various bacterial surface components and extracellular proteins. However, the
precise role of single virulence determinants in relation to infection is hard
to establish. The frequent recovery of staphylococcal isolates that produce
leukocidal toxins from patients with deep skin and soft tissue infections,
particularly furunculosis, cutaneous abscesses, and severe necrotizing
pneumonia, suggests that the Panton-Valentine leukocidin (PVL) is 1 such
virulence factor that has a major role in pathogenicity (1–3).
In 1932, Panton and Valentine described PVL as a virulence
factor belonging to the family of synergohymenotropic toxins (4). These
toxins form pores in the membrane of host defense cells by synergistic action
of 2 secretory proteins, designated LukS-PV and LukF-PV, which are encoded by 2
cotranscribed genes of a prophage integrated in the S. aureus chromosome
(5). PVL is mostly associated with community-acquired
methicillin-resistant S. aureus (MRSA) infections and distinguishable
from nosocomial MRSA by nonmultidrug resistance and carriage of the type IV
staphylococcal chromosome cassette element (SCCmec type IV) (6,7).
Despite the presumed importance of PVL as a virulence
factor, few data are available on its prevalence among S. aureus isolates from the nares of healthy persons compared with stains isolated from
infections. This lack of data led us to investigate the frequency of PVL
gene–positive S. aureus strains obtained from the nares of healthy
carriers in the community. For this purpose, a single polymerase chain reaction
method was used to detect both lukS-PV and lukF-PV genes (2).
In a previous study, the population structure of S.
aureus, isolated from the nares of healthy persons in the Rotterdam area,
the Netherlands, was elucidated (8). Strains were obtained from healthy
children (<19 years) and elderly persons (>55 years). Invasive strains
(blood culture, skin and soft tissue infections, and impetigo isolates) were
included in this study (Table). All carriage and clinical isolates (n = 1,033)
were mecA negative. We used the same strain collection to study the PVL
prevalence in carriage and invasive isolates of S. aureus from a single
geographic region.
Five PVL-positive S. aureus strains (0.6%) were found
in the carriage group (n = 829), and 3 (2.1%) of 146 blood-culture isolates
carried the PVL gene (Table). This finding is in agreement with previously
reported low PVL prevalences by Prevost et al. (0% in 31 carriage isolates and
1.4% in 69 blood-culture isolates) and Von Eiff et al. (1.4% in 210 carriage
isolates and 0.9% in 219 blood-culture isolates) (9,10). However, a higher
prevalence of PVL (38.9%) was found in S. aureus strains causing
abscesses and arthritis (Fisher exact test, p <0.0001) (8). This
finding is also in agreement with the proposed involvement of PVL in severe and
invasive (soft tissue) staphylococcal infections (1–3). No significant
differences were found in the presence of PVL when carriage isolates were
compared with invasive blood-culture isolates. PVL was found in each major
genomic amplified fragment length polymorphism (AFLP) cluster, indicating that
PVL has been introduced in distinct phylogenetic subpopulations of S. aureus (Figure). Multilocus sequence typing analysis of a subset of the strain
collection showed that the 15 PVL-positive strains were within clonal complex
(CC) 30 (n = 7), CC 121 (n = 3), CC 1 (n = 2), CC 8 (n = 1), CC 22 (n = 1), and
CC 45 (n = 1) (Table) (8). Although PVL was found among several
staphylococcal genotypes, it was slightly overrepresented in AFLP cluster IVb
(CC 121) compared with major clusters I and III. Whether the prevalence of PVL
in carriage- and blood-culture isolates is higher and differs among distinct
genetic clusters of S. aureus in countries with endemic CA-MRSA has to
be investigated further.
In conclusion, we have shown that the PVL-encoding phage has
entered distinct staphylococcal lineages, although its prevalence differs per
clonal group. PVL is associated with skin and soft tissue infections but not
with bacteremia, which suggests that PVL is not likely to be involved in the
pathogenesis of bacteremia. Infections caused by PVL-positive S. aureus strains have been documented since the 1930s. Expansion and increased incidence
of such infections, however, are more recent, and further epidemiologic studies
for tracking this phenomenon are still warranted.
References
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Lina G, Bes M, et al. Association between Staphylococcus aureus strains
carrying gene for Panton-Valentine leukocidin and highly lethal necrotising
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- Lina G, Piemont Y, Godail-Gamot F, Bes M, Peter MO,
Gauduchon V, et al. Involvement of Panton-Valentine leukocidin-producing
Staphylococcus aureus in primary skin infections and pneumonia. Clin Infect
Dis. 1999;29:1128–32.
- Holmes A, Ganner M, McGuane S, Pitt TL, Cookson BD, Kearns
AM. Staphylococcus aureus isolates carrying Panton-Valentine leucocidin genes
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clinical disease. J Clin Microbiol. 2005;43:2384–90.
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1932;1:506–8.
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Staphylococcus aureus ATCC 49775 are encoded by distinct genetic loci and have
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Table. Panton-Valentine Leukocidin (PVL) distribution
among carriage and invasive isolates per genetic cluster of Staphylococcus
aureus |
|
| |
Amplified fragment length polymorphism cluster |
|
I
(n = 462) |
II
(n= 261) |
III
(n = 208) |
IVa
(n = 62) |
IVb
(n = 40) |
Total
(N = 1,033) |
|
|
|
|
|
|
PVL positive, n (%) |
|
Carriage isolates
(n = 829) |
1 |
1 |
1 |
0 |
2 |
5 (0.6)* |
Bacteremia isolates
(n = 146) |
1 |
1 |
0 |
0 |
1 |
3 (2.1)† |
Soft tissue infection isolates
(n = 18) |
1 |
5 |
0 |
1 |
0 |
7 (38.9)‡ |
Impetigo isolates
(n = 40) |
0 |
0 |
0 |
0 |
0 |
0 (0.0) |
Total
(N = 1,033) |
3 (0.6)§ |
7 (2.7) |
1 (0.5)¶ |
1 (1.6) |
3 (7.5)# |
15 (1.5) |
MLST** data of PVL-positive isolates |
CC 1, n = 2
CC 8, n = 1 |
CC 30, n = 7 |
CC 45, n = 1 |
CC 22, n = 1 |
CC 121, n = 3 |
|
|
‡versus *Fisher exact test
(2-sided); p<0.0001. |
‡versus †Fisher exact test
(2-sided); p<0.0001. |
#versus §Fisher exact test
(2-sided); p = 0.0079. |
#versus ¶Fisher exact test
(2-sided); p = 0.0140. |
**MLST, multilocus sequence typing; CC, clonal complex. |
Suggested citation
for this article:
Melles DC, van
Leeuwen WB, Boelens HAM, Peeters JK, Verbrugh HA, van Belkum A.
Panton-Valentine leukocidin genes in Staphylococcus aureus [letter]. Emerg Infect
Dis [serial on the Internet]. 2006 Jul [date cited]. Available from
http://www.cdc.gov/ncidod/EID/vol12no07/05-0865.htm
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