The Pediatric Infectious Disease Journal • Volume 34, Number 1, January 2015
REFERENCES 1. Lin PH, Chao TL, Kuo SW, et al. Virological, serological, and antiviral studies in an imported human case of Avian Influenza A(H7N9) virus in Taiwan. Clin Infect Dis. 2014;58: 242–246. 2. Ip DK, Liao Q, Wu P, et al. Detection of mild to moderate influenza A/H7N9 infection by China’s national sentinel surveillance system for influenza-like illness: case series. BMJ. 2013;346:f3693. 3. Cowling BJ, Freeman G, Wong HY, et al. Preliminary inferences on the agespecific seriousness of human disease caused by avian influenza A(H7N9) infections in China, Euro Surveill. 2013;18:20475. 4. Li Q, Zhou L, Zhou M, et al. Preliminary report: epidemiology of the Avian Influenza A (H7N9) outbreak in China. N Engl J Med. 2013;1–11. 5. Merler S, Ajelli M, Camilloni B, et al. Pandemic influenza A/H1N1pdm in Italy: age, risk and population susceptibility. PLoS One. 2013;8:e74785. 6. Zhu YM. A limited understanding of hazard of influenza A virus subtype H7N9 in children. CJCP. 2013;15:409–411.
KINGELLA KINGAE SEQUENCE TYPE-COMPLEX 14 ARTHRITIS IN A 16-MONTH-OLD CHILD IN GREECE Ioanna N. Grivea, MD, PhD,* Aspasia N. Michoula, MD,* Romain Basmaci, MD,†‡ Zoe H. Dailiana, MD, PhD,§ George Tsimitselis, MD,¶ Stéphane Bonacorsi, MD, PhD,†‡ and George A. Syrogiannopoulos, MD, PhD* Abstract: We describe the first case of Kingella kingae arthritis in a 16-month-old girl in Greece, which has been diagnosed by novel molecular techniques. A joint aspiration of her knee was performed before the initiation of antibiotics, as well as on the 5th and 14th day of empiric antimicrobial therapy. The synovial fluid white blood cell count decreased from 65,000 to 1500 cells/mm3, but the percentage of neutrophils remained 90% in all 3 specimens. Molecular analysis of the synovial fluid specimens by realtime polymerase chain reaction and multilocus sequence typing enabled us to reveal the presence of K. kingae belonging to the international sequence type-complex 14, which persisted up to the fifth day of antibiotic therapy. Key Words: Kingella kingae, septic arthritis, real-time polymerase chain reaction, multilocus sequence typing, Greece Accepted for publication July 21, 2014. From the *Departments of Pediatrics, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital, Larissa, Greece; †Univ Paris Diderot, Sorbonne Paris Cité; ‡AP-HP, Laboratoire de Microbiologie, Hôpital Robert-Debré, Paris, France; Departments of §Orthopedic Surgery; and ¶Radiology, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital, Larissa, Greece The authors have no conflicts of interest to disclose. Address for correspondence: George A. Syrogiannopoulos, MD, Department of Pediatrics, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital of Larissa, Biopolis, 411 10 Larissa, Greece. E-mail [email protected]. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com). Copyright © 2014 by Lippincott Williams & Wilkins DOI: 10.1097/INF.0000000000000503
K
ingella kingae is being increasingly recognized as a pathogen responsible for bacteremia and osteoarticular infections among children aged 6–48 months.1–4 With the optimization of conventional culture methods, including the inoculation of synovial fluid into a blood culture vial,1 and the implementation of novel molecular techniques for the synovial fluid analysis,4–6 K. kingae appears to have supplanted Staphylococcus aureus as the primary pathogen responsible for septic arthritis and osteomyelitis in children under 4 years of age in some countries.3–7 However, knowledge among the © 2014 Lippincott Williams & Wilkins
Kingella Arthritis
medical community regarding the incidence and the diagnosis of this organism is insufficient, and K. kingae invasive infections are probably misdiagnosed in a large number of cases. To our knowledge, no cases of K. kingae osteoarticular infection in Greece have been reported in the English literature, probably because of difficulties encountered in the isolation of this pathogen and absence of implementation of specific molecular techniques. In Greece S. aureus, a major pathogen responsible for ostearticular infections,7,8 exhibits increased resistance to methicillin.9 Currently, it is estimated that about one fourth of staphylococcal ostearticular infections are due to Panton–Valentine leukocidin producing methicillin-resistant isolates.10 The latter observation plays an important role in the selection of empiric antibiotic therapy in our country. Improvement of K. kingae diagnosis could facilitate the antimicrobial treatment, especially the oral treatment, as K. kingae is mostly susceptible to beta-lactam antibiotics, such as amoxicillin.1,3 We describe a case of K. kingae arthritis in a toddler living in Central Greece, with special focus on the cytochemical and molecular analysis of the synovial fluid over the course of the disease.
CASE REPORT A 16-month-old girl was referred to the Department of Pediatrics of the University Hospital of Larissa with a 4-day history of fever up to 38.9°C and limping/refusal to walk. Ultrasound examination of the left hip was normal. The first hypothesis was that the child suffered from left hip transient synovitis. She was not attending a day-care center, but her 3-year-old brother was. Within the first day of hospitalization, she improved and started walking and running. There were no objective signs of osteomyelitis or septic arthritis on orthopedic and pediatric examinations. Laboratory evaluation revealed a total peripheral white blood cell (WBC) count of 13,600/mm3, an absolute neutrophil count (ANC) of 5500/mm3, C-reactive protein (CRP) of 39 mg/L and erythrocyte sedimentation rate of 45 mm/h. A blood culture remained sterile. The child defervesced after the third day of hospitalization without antimicrobial or surgical treatment. The girl remained afebrile and free of any signs and symptoms for 48 hours. At that point, the limping reappeared and the child refused to walk. The clinical examination revealed findings in another joint. Increasing erythema, edema and tenderness of the left knee and the perisynovial soft tissue were observed. The differential diagnosis of this afebrile child included septic arthritis, as well as reactive arthritis or inflammatory arthropathies. The magnetic resonance imaging of the left lower limb showed no pathologic findings from the left hip, but effusion of the left knee and intense inflammation of the adjacent soft tissue (Fig., Supplemental Digital Content 1, http://links.lww.com/INF/C68). There was no bone involvement. A transdermal joint aspiration was performed and purulent fluid was obtained (Table 1), but arthrotomy was not performed. Gram stain was negative. Laboratory findings demonstrated a total peripheral WBC count of 19,900/mm3, ANC of 11,600/ mm3, CRP of 98 mg/L and erythrocyte sedimentation rate of 81 mm/hr. TABLE 1. Cytochemical and Molecular Analysis of the Synovial Fluid Over the Course of Kingella kingae Arthritis in a Greek Toddler Specimen, Day of Antibiotic Treatment Before 5th 14th
WBC Count (cells/mm3) 65,000 22,000 1500
Neutrophils Glucose RT-PCR for (%) (mg/dL) K. kingae 90 90 90
9 71 71
Positive Positive Negative
RT-PCR, real-time polymerase chain reaction.
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The Pediatric Infectious Disease Journal • Volume 34, Number 1, January 2015
Empiric antibiotic therapy with cefotaxime and clindamycin was initiated. The child remained afebrile. On the fifth day of treatment, as the articular findings were considered to subside relatively slowly and the etiologic agent remained unknown, a second transdermal joint aspiration was performed (Table 1). The laboratory evaluation, performed on the sixth day of treatment, was as follows: total peripheral WBC count of 8800/mm3, ANC of 2600/mm3 and CRP of 5 mg/L. The empiric antibiotic treatment was not altered as the causative agent remained unknown. All the blood and synovial fluid cultures, including the inoculation of synovial fluid into a BacT/Alert blood culture vial, were reported as being negative. On the 14th day of intravenous antimicrobial therapy, the physical examination revealed the presence of considerable residual amount of joint fluid. A final joint aspiration was performed. The local signs and symptoms subsided gradually. A magnetic resonance imaging was repeated on the 21st day of therapy which showed almost complete resolution of the soft tissue inflammation around the left knee joint (Fig., Supplemental Digital Content 1, http://links.lww.com/INF/C68). In addition, there was significant decrease in the joint effusion and no bone lesions were revealed. The child was discharged with oral cefuroxime axetil for 14 days and had a normal late follow-up at 7 months postdischarge.
MOLECULAR STUDIES The samples of joint fluid were stored at −80°C and were sent later to France, in order to perform real-time polymerase chain reaction for K. kingae according to a previously described method.6 Molecular analysis of the specimens revealed the presence of K. kingae DNA (Table 1). Multilocus sequence typing was performed directly on the joint fluid DNA extract as previously described.11,12 Multilocus sequence typing used the sequence of 6 housekeeping genes, abcZ, adk, aroE, cpn60, gdh and recA. A sequence type (ST) number corresponds to a specific combination of distinct alleles and ST complexes (STcs) regrouped ST with no more than 1 different allele. It was possible to successfully sequence 5 of these 6 genes, but gdh failed to amplify. Although the ST could not be determined, we were able to affiliate our strain to the STc-14.
DISCUSSION The present report indicates the circulation of K. kingae strains among young children in Greece. Molecular study showed that the etiologic agent belonged to STc-14, which together with STc-6 and STc-23, are the 3 most common clones with international dissemination.11 STc-14 K. kingae isolates have been recovered from patients with bacteremia and/or skeletal infections in France and Israel.11,13 The use of molecular techniques enabled us not only to identify the etiologic agent but also its genetic characterization. Persistence of DNA detection over the course of antimicrobial therapy was previously described.6 In our case, real-time polymerase chain reaction detected K. kingae genetic material in the sample of synovial fluid obtained on the fifth day of antimicrobial therapy, but not on the 14th day. Clinicians should be aware that molecular diagnosis is possible even after 1 week of antibiotic treatment. The presence of 90% neutrophils in the synovial fluid 2 weeks after effective intravenous antibiotic therapy indicates that K. kingae arthritis may be followed by persistent intra-articular inflammation. The focal inflammation may not be necessarily reflected on the level of circulating inflammatory markers. An obstacle in further elucidating the natural course of K. kingae disease in young children is the difficulty in identifying low grade bacteremia during the initial, sometimes transient, phase of K. kingae invasive disease.3 Although bone and joint infections are not considered self-limited diseases, transient subtle involvement
108 | www.pidj.com
of the skeletal system during an episode of K kingae bacteremia may occur.3 Had blood cultures not been obtained or had no growth, these children would have probably been diagnosed as suffering from transient synovitis. K. kingae invasive disease, especially bacteremia, appears to remain significantly underdiagnosed because of its subtle initial clinical presentation and the technical difficulties in isolating K. kingae from blood as well as from joint fluid cultures. Expanding the implementation of the novel molecular tools can reveal the burden of K. kingae infection and improve our knowledge and experience with different clinical presentations of K. kingae invasive disease. REFERENCES 1. Yagupsky P. Kingella kingae: from medical rarity to an emerging paediatric pathogen. Lancet Infect Dis. 2004;4:358–367. 2. Dubnov-Raz G, Ephros M, Garty BZ, et al. Invasive pediatric Kingella kingae infections: a nationwide collaborative study. Pediatr Infect Dis J. 2010;29:639–643. 3. Yagupsky P, Porsch E, St Geme JW 3rd. Kingella kingae: an emerging pathogen in young children. Pediatrics. 2011;127:557–565. 4. Ceroni D, Cherkaoui A, Ferey S, et al. Kingella kingae osteoarticular infections in young children: clinical features and contribution of a new specific real-time PCR assay to the diagnosis. J Pediatr Orthop. 2010;30:301–304. 5. Chometon S, Benito Y, Chaker M, et al. Specific real-time polymerase chain reaction places Kingella kingae as the most common cause of osteoarticular infections in young children. Pediatr Infect Dis J. 2007;26:377–381. 6. Ilharreborde B, Bidet P, Lorrot M, et al. New real-time PCR-based method for Kingella kingae DNA detection: application to samples collected from 89 children with acute arthritis. J Clin Microbiol. 2009;47:1837–1841. 7. Basmaci R, Lorrot M, Bidet P, et al. Comparison of clinical and biologic features of Kingella kingae and Staphylococcus aureus arthritis at initial evaluation. Pediatr Infect Dis J 2011;30:902–904. 8. Syrogiannopoulos GA, Nelson JD. Duration of antimicrobial therapy for acute suppurative osteoarticular infections. Lancet. 1988;1:37–40. 9. Katopodis GD, Grivea IN, Tsantsaridou AJ, et al. Fusidic acid and clindamycin resistance in community-associated, methicillin-resistant Staphylococcus aureus infections in children of Central Greece. BMC Infect Dis. 2010;10:351. 10. Sdougkos G, Chini V, Papanastasiou DA, et al. Methicillin-resistant Staphylococcus aureus producing Panton-Valentine leukocidin as a cause of acute osteomyelitis in children. Clin Microbiol Infect. 2007;13:651–654. 11. Basmaci R, Yagupsky P, Ilharreborde B, et al. Multilocus sequence typing and rtxA toxin gene sequencing analysis of Kingella kingae isolates demonstrates genetic diversity and international clones. PLoS One. 2012;7:e38078. 12. Bidet P, Collin E, Basmaci R, et al. Investigation of an outbreak of osteoarticular infections caused by Kingella kingae in a childcare center using molecular techniques. Pediatr Infect Dis J. 2013;32:558–560. 13. Amit U, Porat N, Basmaci R, et al. Genotyping of invasive Kingella kingae isolates reveals predominant clones and association with specific clinical syndromes. Clin Infect Dis. 2012;55:1074–1079.
MINIMAL INHIBITORY CONCENTRATION DRIFT OF GLYCOPEPTIDES AND LINEZOLID AGAINST S. AUREUS AT A CHINESE CHILDREN’S CENTER, 2009–2013 Chun-Mei Jing, MS,*†‡ Wei Xie, BS,*† Yuan Chen, BS,* and Cai Wang, MS,*†‡ Abstract: We analyzed the drift in the minimum inhibitory concentration (MIC) of glycopeptides and linezolid against 793 methicillin-resistant Staphylococcus aureus (MRSA) and 4696 methicillin-susceptible S. aureus (MSSA) isolates from Chinese children. For vancomycin and teicoplanin, no significant change occurred in different years for MIC values ≥ 2 μg/mL, either in MRSA or MSSA. For linezolid, there was an MIC drift in MRSA and in MSSA.
© 2014 Lippincott Williams & Wilkins
REFERENCES 1. Lin PH, Chao TL, Kuo SW, et al. Virological, serological, and antiviral studies in an imported human case of Avian Influenza A(H7N9) virus in Taiwan. Clin Infect Dis. 2014;58: 242–246. 2. Ip DK, Liao Q, Wu P, et al. Detection of mild to moderate influenza A/H7N9 infection by China’s national sentinel surveillance system for influenza-like illness: case series. BMJ. 2013;346:f3693. 3. Cowling BJ, Freeman G, Wong HY, et al. Preliminary inferences on the agespecific seriousness of human disease caused by avian influenza A(H7N9) infections in China, Euro Surveill. 2013;18:20475. 4. Li Q, Zhou L, Zhou M, et al. Preliminary report: epidemiology of the Avian Influenza A (H7N9) outbreak in China. N Engl J Med. 2013;1–11. 5. Merler S, Ajelli M, Camilloni B, et al. Pandemic influenza A/H1N1pdm in Italy: age, risk and population susceptibility. PLoS One. 2013;8:e74785. 6. Zhu YM. A limited understanding of hazard of influenza A virus subtype H7N9 in children. CJCP. 2013;15:409–411.
KINGELLA KINGAE SEQUENCE TYPE-COMPLEX 14 ARTHRITIS IN A 16-MONTH-OLD CHILD IN GREECE Ioanna N. Grivea, MD, PhD,* Aspasia N. Michoula, MD,* Romain Basmaci, MD,†‡ Zoe H. Dailiana, MD, PhD,§ George Tsimitselis, MD,¶ Stéphane Bonacorsi, MD, PhD,†‡ and George A. Syrogiannopoulos, MD, PhD* Abstract: We describe the first case of Kingella kingae arthritis in a 16-month-old girl in Greece, which has been diagnosed by novel molecular techniques. A joint aspiration of her knee was performed before the initiation of antibiotics, as well as on the 5th and 14th day of empiric antimicrobial therapy. The synovial fluid white blood cell count decreased from 65,000 to 1500 cells/mm3, but the percentage of neutrophils remained 90% in all 3 specimens. Molecular analysis of the synovial fluid specimens by realtime polymerase chain reaction and multilocus sequence typing enabled us to reveal the presence of K. kingae belonging to the international sequence type-complex 14, which persisted up to the fifth day of antibiotic therapy. Key Words: Kingella kingae, septic arthritis, real-time polymerase chain reaction, multilocus sequence typing, Greece Accepted for publication July 21, 2014. From the *Departments of Pediatrics, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital, Larissa, Greece; †Univ Paris Diderot, Sorbonne Paris Cité; ‡AP-HP, Laboratoire de Microbiologie, Hôpital Robert-Debré, Paris, France; Departments of §Orthopedic Surgery; and ¶Radiology, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital, Larissa, Greece The authors have no conflicts of interest to disclose. Address for correspondence: George A. Syrogiannopoulos, MD, Department of Pediatrics, University of Thessaly, School of Health Sciences, Faculty of Medicine, General University Hospital of Larissa, Biopolis, 411 10 Larissa, Greece. E-mail [email protected]. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com). Copyright © 2014 by Lippincott Williams & Wilkins DOI: 10.1097/INF.0000000000000503
K
ingella kingae is being increasingly recognized as a pathogen responsible for bacteremia and osteoarticular infections among children aged 6–48 months.1–4 With the optimization of conventional culture methods, including the inoculation of synovial fluid into a blood culture vial,1 and the implementation of novel molecular techniques for the synovial fluid analysis,4–6 K. kingae appears to have supplanted Staphylococcus aureus as the primary pathogen responsible for septic arthritis and osteomyelitis in children under 4 years of age in some countries.3–7 However, knowledge among the © 2014 Lippincott Williams & Wilkins
Kingella Arthritis
medical community regarding the incidence and the diagnosis of this organism is insufficient, and K. kingae invasive infections are probably misdiagnosed in a large number of cases. To our knowledge, no cases of K. kingae osteoarticular infection in Greece have been reported in the English literature, probably because of difficulties encountered in the isolation of this pathogen and absence of implementation of specific molecular techniques. In Greece S. aureus, a major pathogen responsible for ostearticular infections,7,8 exhibits increased resistance to methicillin.9 Currently, it is estimated that about one fourth of staphylococcal ostearticular infections are due to Panton–Valentine leukocidin producing methicillin-resistant isolates.10 The latter observation plays an important role in the selection of empiric antibiotic therapy in our country. Improvement of K. kingae diagnosis could facilitate the antimicrobial treatment, especially the oral treatment, as K. kingae is mostly susceptible to beta-lactam antibiotics, such as amoxicillin.1,3 We describe a case of K. kingae arthritis in a toddler living in Central Greece, with special focus on the cytochemical and molecular analysis of the synovial fluid over the course of the disease.
CASE REPORT A 16-month-old girl was referred to the Department of Pediatrics of the University Hospital of Larissa with a 4-day history of fever up to 38.9°C and limping/refusal to walk. Ultrasound examination of the left hip was normal. The first hypothesis was that the child suffered from left hip transient synovitis. She was not attending a day-care center, but her 3-year-old brother was. Within the first day of hospitalization, she improved and started walking and running. There were no objective signs of osteomyelitis or septic arthritis on orthopedic and pediatric examinations. Laboratory evaluation revealed a total peripheral white blood cell (WBC) count of 13,600/mm3, an absolute neutrophil count (ANC) of 5500/mm3, C-reactive protein (CRP) of 39 mg/L and erythrocyte sedimentation rate of 45 mm/h. A blood culture remained sterile. The child defervesced after the third day of hospitalization without antimicrobial or surgical treatment. The girl remained afebrile and free of any signs and symptoms for 48 hours. At that point, the limping reappeared and the child refused to walk. The clinical examination revealed findings in another joint. Increasing erythema, edema and tenderness of the left knee and the perisynovial soft tissue were observed. The differential diagnosis of this afebrile child included septic arthritis, as well as reactive arthritis or inflammatory arthropathies. The magnetic resonance imaging of the left lower limb showed no pathologic findings from the left hip, but effusion of the left knee and intense inflammation of the adjacent soft tissue (Fig., Supplemental Digital Content 1, http://links.lww.com/INF/C68). There was no bone involvement. A transdermal joint aspiration was performed and purulent fluid was obtained (Table 1), but arthrotomy was not performed. Gram stain was negative. Laboratory findings demonstrated a total peripheral WBC count of 19,900/mm3, ANC of 11,600/ mm3, CRP of 98 mg/L and erythrocyte sedimentation rate of 81 mm/hr. TABLE 1. Cytochemical and Molecular Analysis of the Synovial Fluid Over the Course of Kingella kingae Arthritis in a Greek Toddler Specimen, Day of Antibiotic Treatment Before 5th 14th
WBC Count (cells/mm3) 65,000 22,000 1500
Neutrophils Glucose RT-PCR for (%) (mg/dL) K. kingae 90 90 90
9 71 71
Positive Positive Negative
RT-PCR, real-time polymerase chain reaction.
www.pidj.com | 107
Grivea et al
The Pediatric Infectious Disease Journal • Volume 34, Number 1, January 2015
Empiric antibiotic therapy with cefotaxime and clindamycin was initiated. The child remained afebrile. On the fifth day of treatment, as the articular findings were considered to subside relatively slowly and the etiologic agent remained unknown, a second transdermal joint aspiration was performed (Table 1). The laboratory evaluation, performed on the sixth day of treatment, was as follows: total peripheral WBC count of 8800/mm3, ANC of 2600/mm3 and CRP of 5 mg/L. The empiric antibiotic treatment was not altered as the causative agent remained unknown. All the blood and synovial fluid cultures, including the inoculation of synovial fluid into a BacT/Alert blood culture vial, were reported as being negative. On the 14th day of intravenous antimicrobial therapy, the physical examination revealed the presence of considerable residual amount of joint fluid. A final joint aspiration was performed. The local signs and symptoms subsided gradually. A magnetic resonance imaging was repeated on the 21st day of therapy which showed almost complete resolution of the soft tissue inflammation around the left knee joint (Fig., Supplemental Digital Content 1, http://links.lww.com/INF/C68). In addition, there was significant decrease in the joint effusion and no bone lesions were revealed. The child was discharged with oral cefuroxime axetil for 14 days and had a normal late follow-up at 7 months postdischarge.
MOLECULAR STUDIES The samples of joint fluid were stored at −80°C and were sent later to France, in order to perform real-time polymerase chain reaction for K. kingae according to a previously described method.6 Molecular analysis of the specimens revealed the presence of K. kingae DNA (Table 1). Multilocus sequence typing was performed directly on the joint fluid DNA extract as previously described.11,12 Multilocus sequence typing used the sequence of 6 housekeeping genes, abcZ, adk, aroE, cpn60, gdh and recA. A sequence type (ST) number corresponds to a specific combination of distinct alleles and ST complexes (STcs) regrouped ST with no more than 1 different allele. It was possible to successfully sequence 5 of these 6 genes, but gdh failed to amplify. Although the ST could not be determined, we were able to affiliate our strain to the STc-14.
DISCUSSION The present report indicates the circulation of K. kingae strains among young children in Greece. Molecular study showed that the etiologic agent belonged to STc-14, which together with STc-6 and STc-23, are the 3 most common clones with international dissemination.11 STc-14 K. kingae isolates have been recovered from patients with bacteremia and/or skeletal infections in France and Israel.11,13 The use of molecular techniques enabled us not only to identify the etiologic agent but also its genetic characterization. Persistence of DNA detection over the course of antimicrobial therapy was previously described.6 In our case, real-time polymerase chain reaction detected K. kingae genetic material in the sample of synovial fluid obtained on the fifth day of antimicrobial therapy, but not on the 14th day. Clinicians should be aware that molecular diagnosis is possible even after 1 week of antibiotic treatment. The presence of 90% neutrophils in the synovial fluid 2 weeks after effective intravenous antibiotic therapy indicates that K. kingae arthritis may be followed by persistent intra-articular inflammation. The focal inflammation may not be necessarily reflected on the level of circulating inflammatory markers. An obstacle in further elucidating the natural course of K. kingae disease in young children is the difficulty in identifying low grade bacteremia during the initial, sometimes transient, phase of K. kingae invasive disease.3 Although bone and joint infections are not considered self-limited diseases, transient subtle involvement
108 | www.pidj.com
of the skeletal system during an episode of K kingae bacteremia may occur.3 Had blood cultures not been obtained or had no growth, these children would have probably been diagnosed as suffering from transient synovitis. K. kingae invasive disease, especially bacteremia, appears to remain significantly underdiagnosed because of its subtle initial clinical presentation and the technical difficulties in isolating K. kingae from blood as well as from joint fluid cultures. Expanding the implementation of the novel molecular tools can reveal the burden of K. kingae infection and improve our knowledge and experience with different clinical presentations of K. kingae invasive disease. REFERENCES 1. Yagupsky P. Kingella kingae: from medical rarity to an emerging paediatric pathogen. Lancet Infect Dis. 2004;4:358–367. 2. Dubnov-Raz G, Ephros M, Garty BZ, et al. Invasive pediatric Kingella kingae infections: a nationwide collaborative study. Pediatr Infect Dis J. 2010;29:639–643. 3. Yagupsky P, Porsch E, St Geme JW 3rd. Kingella kingae: an emerging pathogen in young children. Pediatrics. 2011;127:557–565. 4. Ceroni D, Cherkaoui A, Ferey S, et al. Kingella kingae osteoarticular infections in young children: clinical features and contribution of a new specific real-time PCR assay to the diagnosis. J Pediatr Orthop. 2010;30:301–304. 5. Chometon S, Benito Y, Chaker M, et al. Specific real-time polymerase chain reaction places Kingella kingae as the most common cause of osteoarticular infections in young children. Pediatr Infect Dis J. 2007;26:377–381. 6. Ilharreborde B, Bidet P, Lorrot M, et al. New real-time PCR-based method for Kingella kingae DNA detection: application to samples collected from 89 children with acute arthritis. J Clin Microbiol. 2009;47:1837–1841. 7. Basmaci R, Lorrot M, Bidet P, et al. Comparison of clinical and biologic features of Kingella kingae and Staphylococcus aureus arthritis at initial evaluation. Pediatr Infect Dis J 2011;30:902–904. 8. Syrogiannopoulos GA, Nelson JD. Duration of antimicrobial therapy for acute suppurative osteoarticular infections. Lancet. 1988;1:37–40. 9. Katopodis GD, Grivea IN, Tsantsaridou AJ, et al. Fusidic acid and clindamycin resistance in community-associated, methicillin-resistant Staphylococcus aureus infections in children of Central Greece. BMC Infect Dis. 2010;10:351. 10. Sdougkos G, Chini V, Papanastasiou DA, et al. Methicillin-resistant Staphylococcus aureus producing Panton-Valentine leukocidin as a cause of acute osteomyelitis in children. Clin Microbiol Infect. 2007;13:651–654. 11. Basmaci R, Yagupsky P, Ilharreborde B, et al. Multilocus sequence typing and rtxA toxin gene sequencing analysis of Kingella kingae isolates demonstrates genetic diversity and international clones. PLoS One. 2012;7:e38078. 12. Bidet P, Collin E, Basmaci R, et al. Investigation of an outbreak of osteoarticular infections caused by Kingella kingae in a childcare center using molecular techniques. Pediatr Infect Dis J. 2013;32:558–560. 13. Amit U, Porat N, Basmaci R, et al. Genotyping of invasive Kingella kingae isolates reveals predominant clones and association with specific clinical syndromes. Clin Infect Dis. 2012;55:1074–1079.
MINIMAL INHIBITORY CONCENTRATION DRIFT OF GLYCOPEPTIDES AND LINEZOLID AGAINST S. AUREUS AT A CHINESE CHILDREN’S CENTER, 2009–2013 Chun-Mei Jing, MS,*†‡ Wei Xie, BS,*† Yuan Chen, BS,* and Cai Wang, MS,*†‡ Abstract: We analyzed the drift in the minimum inhibitory concentration (MIC) of glycopeptides and linezolid against 793 methicillin-resistant Staphylococcus aureus (MRSA) and 4696 methicillin-susceptible S. aureus (MSSA) isolates from Chinese children. For vancomycin and teicoplanin, no significant change occurred in different years for MIC values ≥ 2 μg/mL, either in MRSA or MSSA. For linezolid, there was an MIC drift in MRSA and in MSSA.
© 2014 Lippincott Williams & Wilkins
