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Letter
Panton-Valentine Leukocidin–positive
Staphylococcus aureus, Singapore
Li-Yang Hsu,*
Tse-Hsien Koh,* Devanand Anantham,* Asok Kurup,* Kenneth Ping Wah Chan,*
and Ban-Hock Tan*
*Singapore General Hospital, Singapore
Suggested citation
for this article:
Hsu LY, Koh TS, Anantham D, Kurup A, Chan KP, Tan BH. Panton-Valentine
leukocidin-positive Staphylococcus aureus, Singapore [letter].
Emerg Infect Dis [serial on the Internet]. 2004 Aug [date cited].
Available from: http://www.cdc.gov/ncidod/EID/vol10no8/03-1088.htm
To the Editor: Necrotizing community-acquired pneumonia attributable
to Panton-Valentine leukocidin–producing strains of Staphylococcus
aureus has been described as a distinct clinical syndrome with a high
death rate in young, immunocompetent patients (1,2).
This letter details the first reported case of necrotizing pneumonia caused
by Panton-Valentine leukocidin-positive S. aureus in a southeastern
Asian country, Singapore.
An 18-year-old girl of Chinese ethnicity with a 4-day history of fever,
cough, hemoptysis, and dyspnea sought treatment at Singapore General Hospital
in October 2003. This episode had immediately followed an influenza-like
prodromal illness for which a general practitioner had prescribed oral
erythromycin ethinylsuccinate and medications for symptomatic relief.
Her medical history showed an intrauterine Toxoplasma gondii infection
that had resulted in developmental delay and slight mental retardation.
She had never traveled outside Singapore.
On admission, the patient's temperature was 38.4°C, blood pressure
was 130/70 mm Hg, and her pulse rate was 108 per min. Bibasal crackles
were heard on auscultation of her lung fields, and her respiratory rate
was 30 per min despite the use of supplemental oxygen. The results of
physical examination were otherwise unremarkable. Initial chest x-ray
showed air-space shadowing of the right upper and middle lobes of the
lung, as well as blunting of the right costophrenic angle. Blood tests
gave the following results: leukocyte count 7.42 x 109/L, neutrophil
count 6.53 x 109/L, platelet count 287 x 109/L,
hemoglobin level 8.6 g/dL, prothrombin time 15.3 s, and activated partial
thromboplastin time 28.7 s. She was experiencing acute renal failure with
a serum creatinine level of 783 µmol/L. Liver biochemistry was abnormal
with the following values: alkaline phosphatase 513 U/L, alanine aminotransferase
38 U/L, and aspartate aminotransferase 65 U/L. Serum bilirubin level was
within the normal range.
The patient was prescribed intravenous ceftriaxone and azithromycin,
and hemodialysis was initiated. Within 6 hours of hospitalization, the
patient became hypotensive and hypoxemic and required inotropic support
and mechanical ventilation. Intravenous ceftazidime and high-dose cloxacillin
were substituted for ceftriaxone at that time. Blood cultures obtained
on admission were sterile, but penicillin-resistant S. aureus grew
from cultures of aspirated endotracheal tube secretions. Results of immunofluorescent
tests conducted on bronchial washings for viral antigens of influenza
virus A and B, parainfluenza virus, respiratory syncytial virus, and adenovirus
were negative. Computed tomographic scan of the thorax on day 3 of hospitalization
showed widespread confluent consolidation of the right lung with right
pleural effusion and patchy consolidation of the lingular lobe of the
left lung. The total leukocyte count increased to 26.3 x 109/L,
and disseminated intravascular coagulopathy developed. Results of repeated
blood and endotracheal cultures were positive for S. aureus, and
intravenous gentamicin and rifampicin were added to her antimicrobial
cocktail. A transthoracic echocardiogram showed a normal heart with no
evidence of endocarditis.
Despite aggressive support, the patient's condition continued to deteriorate.
A hemopyopneumothorax developed on the right side on day 4 of hospitalization,
which required chest tube insertion. Hemoptysis persisted, and inotropic
and ventilatory requirements progressively increased. The patient died
on day 20 of hospitalization.
The severity of the patient's infection and the clinical symptoms suggested
the presence of Panton-Valentine leukocidin genes in the causative S.
aureus; tests confirmed the suspicion. S. aureus was identified
on the basis of colony morphologic characteristics, the coagulation of
citrated rabbit plasma (bioMérieux, Marcy l'Etoile, France), and production
of a clumping factor (Staphyslide test; bioMérieux). DNA was extracted
from cultures grown on agar plates and amplified following a previously
described protocol (1). The following oligonucleotide
primer sequences were used: luk-PV1, 5´-ATCATTAGGTAAAATGTCTGGACATGATCCA-3´;
luk-PV2, 5´-GCATCAAGTGTATTGGATAGCAAAAGC-3´. Polymerase
chain reaction products were sequenced commercially and submitted to GenBank
(accession no. AY508231).
This case is the first in Singapore of community-acquired pneumonia caused
by S. aureus in which an attempt was made to detect Panton-Valentine
leukocidin genes. Given that the patient had not traveled, she likely
acquired the lethal strain of Panton-Valentine leukocidin–positive S.
aureus locally. This idea is further supported by a recent study which
reported that the Panton-Valentine leukocidin gene is found worldwide,
albeit in community-acquired strains of methicillin-resistant S. aureus
(3).
The incidence of severe community-acquired pneumonia attributable to
Panton-Valentine leukocidin–positive S. aureus is unknown in many
parts of the world. With one exception (4), cases of
Panton-Valentine leukocidin–positive S. aureus causing community-acquired
pneumonia have been reported sporadically only from European countries
and the United States (1,2,5–8). These results may be
attributable to the lack of recognition rather than to the rarity of the
condition. A previous report showed that 7.6% of cases of severe community-acquired
pneumonia in patients requiring ventilatory support in Singapore were
caused by S. aureus (9), and a large proportion
of these would fit the clinical syndrome described by Gillet et al. (2).
Given the ease of transmitting the infection to close contacts (7,10),
with the real possibility of a consequent outbreak (10),
Panton-Valentine leukocidin testing should be conducted on S. aureus
strains isolated from all patients with community-acquired necrotizing
pneumonia and furunculosis for infection control purposes. Implementing
standard hospital methicillin-resistant S. aureus measures resulted
in control of the outbreak described by Boubaker et al. (10).
This measure seems especially relevant given the dismal prognosis offered
by conventional therapy in which the death rate of patients with necrotizing
pneumonia may reach 75% (2). Further research on the
epidemiology, optimal therapy, and prevention of this infection is needed.
References
- Lina G, Piémont 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.
- Gillet Y, Issartel B, Vanhems P, Fournet JC, Lina G, Bes M, et al.
Association
between Staphylococcus aureus strains carrying gene for Panton-Valentine
leukocidin and highly lethal necrotising pneumonia in young immunocompetent
patients. Lancet. 2002; 359:753–9.
- Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H,
et al. Community-acquired
methicillin-resistant Staphylococcus aureus carrying Panton-Valentine
leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003;8:978–84.
- Miyashita T, Shimamoto Y, Nishiya H, Koshibu Y, Sugiyama H, Ono Y,
et al. Destructive
pulmonary embolism in a patient with community-acquired staphylococcal
bacteremia. J Infect Chemother. 2002;8:99–102.
- Boussard V, Parrot A, Mayaud C, Wislez M, Antoine M, Picard C, et
al. Life-threatening
hemoptysis in adults with community-acquired pneumonia due to Panton-Valentine
leukocidin–secreting Staphylococcus aureus. Intensive Care
Med. 2003;29:1840–3.
- Klein JL, Petrovic Z, Treacher D, Edgeworth J. Severe
community-acquired pneumonia caused by Panton-Valentine leukocidin–positive
Staphylococcus aureus: first reported case in the United Kingdom.
Intensive Care Med. 2003;29:1399.
- Osterlund A, Kahlmeter G, Bieber L, Runehagen A, Breider JM. Intrafamilial
spread of highly virulent Staphylococcus aureus strains carrying
the gene for Panton-Valentine leukocidin. Scand J Infect Dis. 2002;34:763–4.
- Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne
J, et al. Comparison
of community- and health care-associated methicillin-resistant Staphylococcus
aureus infection. JAMA. 2003;290:2976–84.
- Tan YK, Khoo KL, Chin SP, Ong YY. Aetiology
and outcome of severe community-acquired pneumonia in Singapore.
Eur Respir J. 1998;12:113–5.
- Boubaker K, Diebold P, Blanc DS, Vandenesch F, Praz G, Dupuis G, et
al. Panton-Valentine
leukocidin and staphylococcal skin infections in schoolchildren.
Emerg Infect Dis. 2004;10:121–4.
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