Panton-Valentine Leukocidin–producing Staphylococcus aureus
http://www.100md.com
《传染病的形成》
Hadassah-Hebrew University Medical Center, Jerusalem, Israel
Ministry of Health, Jerusalem, Israel
During a period of 6 months, a cluster of S. aureus skin and soft tissue infections occurred in 2 families in Jerusalem, Israel, that were related through the mothers, who are sisters. The event started with the 4-year-old boy of family A, who had 5 episodes of skin infections, including 2 episodes of perianal abscesses that required drainage and hospitalization. Culture of pus grew MSSA that was resistant to erythromycin and clindamycin. Subsequently, recurrent abscesses and cellulitis developed in the boy's father's legs, and his mother had severe periorbital cellulitis that required hospitalization and surgical drainage. Approximately 1 month later, a 9-year-old boy in family B had severe cellulitis and abscess around his knee that required hospitalization and surgical drainage. Subsequently, infections developed in 2 more children in family B: 1 had a finger pulp-space infection and the other cellulitis of the lower abdomen. All pus cultures grew S. aureus with identical susceptibility patterns. The cases are summarized in the Table.
Following these events, the families consulted the infectious diseases clinic at the Hadassah-Hebrew University Medical Center in Jerusalem. Since the clinical isolates were not available, nasal cultures were obtained from all family members. S. aureus was isolated from all the affected members of family A and from the parents and the 2 boys in family B. All 7 isolates were subjected to pulsed-field gel electrophoresis (PFGE) after digestion with SmaI. All except 1 had identical band patterns and the same antimicrobial drug susceptibilities as the clinical isolates. The presence of PVL genes was examined by PCR as previously described (2) and was detected only in the isolates with identical PFGE patterns. The families were advised to apply mupirocin nasal ointment twice a day for 5 days and to bathe with 4% chlorhexidine scrub for 1 week (7). At 7 months of follow-up, no new cases of skin infection had occurred in either family. An epidemiologic investigation was undertaken by the local department of health to determine if 3 kindergartens and 2 schools attended by the 7 children had an increased incidence of staphylococcal skin disease. No evidence of unusual disease was found.
We describe here the first confirmed cases of PVL-producing S. aureus infections in Israel. Maier et al (8) recently described 2 cases of similar infections that occurred in German tourists after visiting the Dead Sea area, but since these infections were caused by MRSA, it is probable that the isolates were genetically distinct from the strain described here. In addition, to the best of our knowledge this is the first description of transmission of PVL-producing MSSA between related families. Previous reports described community-related outbreaks that occurred within families (6,8,9), between schoolmates (4), and between football team players (10). The exact route of transmission was not identified in some of these cases but it was presumed to have been close contact leading to skin (10) or nasal (4) colonization and subsequent active infection. In our report, the PVL-producing S. aureus clone was detected in nasal cultures in 6 of the 11 members of the 2 families. In this niche, it was able to persist and cause a series of infections in a relatively large number of family members. Even though the S. aureus isolated from active lesions were not available for testing, the recovery of identical PVL-positive organisms from nasal cultures strongly suggests the presence of a pathogenic clone that probably caused the recurrent infections in the 6 affected family members. Our investigation highlights the high transmissibility of this PVL-producing S. aureus clone, its high attack rate, and its virulence. The intervention in this outbreak might have prevented not only subsequent recurrences of cutaneous infections but also further spread of this clone and the manifestation of even more serious infections such as necrotizing pneumonia. Increasing awareness among community-based healthcare providers of PVL-producing S. aureus infections is important to facilitate rapid and adequate response in similar clinical events in the future.
References
Genestier AL, Michalete MC, Prevoset G, Bellot G, Chalabreysse L, Peyrol S, et al. Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils. J Clin Invest. 2005;115:3117–27.
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.
Vandenesch F, Naimi T, Enright MC, Lina G, Nimma GR, Heffernan H, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003;9:978–84.
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.
sterlund 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;34:763–87.
Le Thomas I, Mariani-Kurkdjian P, Collignon A, Gravet A, Clermont O, Brahimi N, et al. Breast milk transmission of a Panton-Valentine leukocidin–producing Staphylococcus aureus strain causing infantile pneumonia. J Clin Microbiol. 2001;39:728–9.
Morreilon P, Que YA, Glauser MP. Staphylococcus aureus. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005. p. 2338.
Maier J, Melzl H, Reischl U, Drubel I, Witte W, Lehn N, et al. Panton-Valentine leukocidin-positive methicillin-resistant Staphylococcus aureus in Germany associated with travel or foreign family origin. Eur J Clin Microbiol Infect Dis. 2005;24:637–9.
Jones TF, Creech CB, Erwin P, Baird SG, Woron AM, Schaffner W. Family outbreaks of invasive community-associated methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis. 2006;42:e76–8.
Begier EM, Frenette K, Barrett NL, Mshar P, Petit S, Boxrud DJ, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39:1446–53.(Amos Adler, Violeta Tempe)
Ministry of Health, Jerusalem, Israel
During a period of 6 months, a cluster of S. aureus skin and soft tissue infections occurred in 2 families in Jerusalem, Israel, that were related through the mothers, who are sisters. The event started with the 4-year-old boy of family A, who had 5 episodes of skin infections, including 2 episodes of perianal abscesses that required drainage and hospitalization. Culture of pus grew MSSA that was resistant to erythromycin and clindamycin. Subsequently, recurrent abscesses and cellulitis developed in the boy's father's legs, and his mother had severe periorbital cellulitis that required hospitalization and surgical drainage. Approximately 1 month later, a 9-year-old boy in family B had severe cellulitis and abscess around his knee that required hospitalization and surgical drainage. Subsequently, infections developed in 2 more children in family B: 1 had a finger pulp-space infection and the other cellulitis of the lower abdomen. All pus cultures grew S. aureus with identical susceptibility patterns. The cases are summarized in the Table.
Following these events, the families consulted the infectious diseases clinic at the Hadassah-Hebrew University Medical Center in Jerusalem. Since the clinical isolates were not available, nasal cultures were obtained from all family members. S. aureus was isolated from all the affected members of family A and from the parents and the 2 boys in family B. All 7 isolates were subjected to pulsed-field gel electrophoresis (PFGE) after digestion with SmaI. All except 1 had identical band patterns and the same antimicrobial drug susceptibilities as the clinical isolates. The presence of PVL genes was examined by PCR as previously described (2) and was detected only in the isolates with identical PFGE patterns. The families were advised to apply mupirocin nasal ointment twice a day for 5 days and to bathe with 4% chlorhexidine scrub for 1 week (7). At 7 months of follow-up, no new cases of skin infection had occurred in either family. An epidemiologic investigation was undertaken by the local department of health to determine if 3 kindergartens and 2 schools attended by the 7 children had an increased incidence of staphylococcal skin disease. No evidence of unusual disease was found.
We describe here the first confirmed cases of PVL-producing S. aureus infections in Israel. Maier et al (8) recently described 2 cases of similar infections that occurred in German tourists after visiting the Dead Sea area, but since these infections were caused by MRSA, it is probable that the isolates were genetically distinct from the strain described here. In addition, to the best of our knowledge this is the first description of transmission of PVL-producing MSSA between related families. Previous reports described community-related outbreaks that occurred within families (6,8,9), between schoolmates (4), and between football team players (10). The exact route of transmission was not identified in some of these cases but it was presumed to have been close contact leading to skin (10) or nasal (4) colonization and subsequent active infection. In our report, the PVL-producing S. aureus clone was detected in nasal cultures in 6 of the 11 members of the 2 families. In this niche, it was able to persist and cause a series of infections in a relatively large number of family members. Even though the S. aureus isolated from active lesions were not available for testing, the recovery of identical PVL-positive organisms from nasal cultures strongly suggests the presence of a pathogenic clone that probably caused the recurrent infections in the 6 affected family members. Our investigation highlights the high transmissibility of this PVL-producing S. aureus clone, its high attack rate, and its virulence. The intervention in this outbreak might have prevented not only subsequent recurrences of cutaneous infections but also further spread of this clone and the manifestation of even more serious infections such as necrotizing pneumonia. Increasing awareness among community-based healthcare providers of PVL-producing S. aureus infections is important to facilitate rapid and adequate response in similar clinical events in the future.
References
Genestier AL, Michalete MC, Prevoset G, Bellot G, Chalabreysse L, Peyrol S, et al. Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils. J Clin Invest. 2005;115:3117–27.
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.
Vandenesch F, Naimi T, Enright MC, Lina G, Nimma GR, Heffernan H, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003;9:978–84.
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.
sterlund 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;34:763–87.
Le Thomas I, Mariani-Kurkdjian P, Collignon A, Gravet A, Clermont O, Brahimi N, et al. Breast milk transmission of a Panton-Valentine leukocidin–producing Staphylococcus aureus strain causing infantile pneumonia. J Clin Microbiol. 2001;39:728–9.
Morreilon P, Que YA, Glauser MP. Staphylococcus aureus. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 6th ed. Philadelphia: Elsevier Churchill Livingstone; 2005. p. 2338.
Maier J, Melzl H, Reischl U, Drubel I, Witte W, Lehn N, et al. Panton-Valentine leukocidin-positive methicillin-resistant Staphylococcus aureus in Germany associated with travel or foreign family origin. Eur J Clin Microbiol Infect Dis. 2005;24:637–9.
Jones TF, Creech CB, Erwin P, Baird SG, Woron AM, Schaffner W. Family outbreaks of invasive community-associated methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis. 2006;42:e76–8.
Begier EM, Frenette K, Barrett NL, Mshar P, Petit S, Boxrud DJ, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39:1446–53.(Amos Adler, Violeta Tempe)