3.2 Predisposition and risk factors
We did not identify any somatic predisposing conditions in our 6 patients. No patient had sickle cell disease and all patients had no immune deficiency and were healthy before the occurrence of this infection.
3.3 Laboratory findings
The median C-reactive protein (CRP) on admission was 274 mg/L (159–371). CRP was at its highest on admission for all patients. Five patients had leukocytosis with polymorphonucleosis.
3.4 Imaging results
All patients had a plain radiography after admission, and an injected MRI. Five out of 6 children had an echocardiography: 2 pericarditis were confirmed. One patient underwent a scintigraphy in Martinique, to identify multiple lesions. Four children with acute osteomyelitis had a subperiosteal abscess.
3.5 Surgical interventions
All patients underwent surgery. A surgical drainage by arthrotomy was performed for 2 children: knee and ankle septic arthritis. Needle aspiration and drainage was needed for the other 4 patients who suffered from acute osteomyelitis (Fig. 1A and B).
3.6 Microbiological results
The isolation of a microorganism was possible in all cases. All 6 cases had a blood culture that came back positive for MSSA within 24 to 48 hours. In 3 out of 6 cases, the pus culture was positive for MSSA. One patient with a necrotizing pneumonia had a positive sputum culture for MSSA. The median time of negativization of blood cultures was 10 days.
Empirical intravenous therapy including an antibiotic active against MSSA was started on admission. Two children received amoxicillin-clavulanate combined to gentamicin. Three children received cefotaxime combined to gentamicin. One child received ceftriaxone and amikacin. Clindamycin, that was shown to have an in vitro antitoxin effect, completed the therapy within 3 days for all patients. Subsequent oral therapy consisted of either ciprofloxacine and rifampicin, or clindamycin and rifampicin. Duration of oral therapy was of ≥6 weeks.
3.8 Follow-up and outcome, complications, and sequelae
Apyrexia was obtained for all patients within a mean of 12 days (8–16). One patient presented on admission with a septic thrombophlebitis of the femoral-popliteal vein. Three patients had secondary visceral complications: 2 cases of necrotizing pneumonia and 2 pericarditis. One had a pyomyositis and another died of cardiac tamponade. One developed a chronic osteomyelitis and suffered from functional impairment.
The clinical cases described in our study have in common a particularly severe presentation with a very high CRP and sometimes signs of septic shock with pneumonia or pericarditis. An extension of the infection or the formation of abscesses were also characteristic. Patient 4, who had a particularly severe plurifocal infection, has been transferred to a university reference hospital in Martinique, for orthopedic and cardiac care. Despite a favorable clinical course, the patient still has motor sequelae. Patient 1 died of tamponade during the pericardial puncture. These results are consistent with published studies.[10–14] The MRI thus plays an important role in the diagnosis but especially in the preoperative assessment to estimate the extent of the infection. As stated in most studies, intravenous empiric antibiotics against SA and its toxins, given after a early and aggressive surgical management, seem to be a key point in the treatment.[10–14] Indeed, drainage and washes repetition is often necessary to overcome the infection. But in our study, only one child underwent multiple surgeries. These SA-LPV infections can be life-threatening and are at high risk of complications and sequalae. The comparison with 4 studies,[7,11–13] publishing clinical cases like ours, shows similarities, with the only difference that, unlike our study, there was no death. Even though French Guiana, which is a European region, is located in South America, our study reported a considerably lower proportion of MRSA. In the United States, the proportion of PVL-producing SA was consistently higher in infections caused by MRSA (74%–100%) than those caused by MSSA (9%–46%). The studies performed outside the United States, except in Greece, that included osteoarticular infections caused by both MSSA and MRSA, have reported a considerably lower proportion of MRSA. The high rate of MRSA is not linked to severity. Indeed, Gillet et al demonstrated that severity is linked with PVL secretion more than with resistance.
Our results have some limitations: first, we know neither the number of PVL-positive cases that are treated in primary institutions nor the proportion of SA strains referred for PVL testing. We can thus expect that the number of BJI due to PVL-positive SA in French Guiana is currently probably underestimated. One might wonder if these infections would not be more common in tropical environments, where climatic factors might favor them. However, there was no information regarding the patients’ living conditions. Second, the rate of MRSA in the pediatric population seems very low in French Guiana. If the prevalence of PVL-producing strains depends on the prevalence of MRSA, this absence of MRSA in our study might play a role in the distribution of PVL in our region.
BJI due to SA-PLV seems to be more severe. In front of a severe acute osteomyelitis or arthritis, it is essential to look for the toxin, to perform MRI to estimate the extent of the infection. If not recognized, such infection can progress to septic shock, or even the death of the patient. Intravenous empiric antibiotics against SA and its toxins, given after an early and aggressive surgical management, seem to be a key point in the treatment. Given the high risk of complications, multidisciplinary management including aggressive surgical treatment is necessary.
Conceptualization: Narcisse Elenga, Coralie Hardy, Lindsay Osei.
Data curation: Coralie Hardy, Lindsay Osei, Thierry Basset.
Investigation: Narcisse Elenga, Coralie Hardy.
Methodology: Narcisse Elenga, Thierry Basset.
Supervision: Narcisse Elenga.
Validation: Narcisse Elenga, Lindsay Osei.
Visualization: Thierry Basset.
Writing – original draft: Coralie Hardy.
Writing – review and editing: Narcisse Elenga, Lindsay Osei, Thierry Basset.
. Iliadis AD, Ramachandran M. Paediatric bone and joint infection. EFORT Open Rev 2017;2:7–12.
. Osei L, El Houmami N, Minodier P, et al. Paediatric bone and joint infections
in French Guiana
: a 6 year retrospective review. J Trop Pediatr 2017;63:380–8.
. Dohin B, Gillet Y, Kohler R, et al. Pediatric bone and joint infections
caused by Panton-Valentine leukocidin-positive Staphylococcus aureus. Pediatr Infect Dis J 2007;26:1042–8.
. Bocchini CE, Hulten KG, Mason EO Jr, et al. Panton-Valentine leukocidin genes are associated with enhanced inflammatory response and local disease in acute hematogenous Staphylococcus aureus osteomyelitis in children. Pediatrics 2006;117:433–40.
. Otto M. Staphylococcus aureus tsoxins. Curr Opin Microbiol 2013;17:32–7.
. Spaan AN, van Strijp JAG, Torres VJ. Leukocidins: staphylococcal bi-component pore-forming toxins find their receptors. Nat Rev Microbiol 2017;15:435–47.
. Gillet Y, Dohin B, Dumitrescu O, et al. Osteoarticular infections with staphylococcus aureus secreting Panton-Valentine Leucocidin. Arch Pediatr 2007;14(Suppl. 2):S102–7.
. Labbé JL, Peres O, Leclair O. Acute osteomyelitis in children: the pathogenesis revisited? Orthop Traumatol Surg Res 2010;96:268–75.
. Saavedra-Lozano J, Falup-Pecurariu O, Faust SN, et al. Bone and joint infections
. Pediatr Infect Dis J 2017;36:788–99.
. Mitchell PD, Hunt DM, Lyall H, et al. Panton-Valentine leukocidin-secreting Staphylococcus aureus causing severe musculoskeletal sepsis in children. A new threat. J Bone Joint Surg Br 2007;89:1239–42.
. Didisheim C, Dubois-Ferrière V, Dhouib A, et al. Severe osteoarticular infections with Staphylococcus aureus producer of Panton-Valentine Leukocidine in children. Rev Med Suisse 2014;10:355–9.
. Machuca MA, González CI, Sosa LM. Methicillin-resistant Staphylococcus aureus causes both community-associated and health care-associated infections in children at the Hospital Universitario de Santander. Biomedica 2014;34(Suppl. 1):163–9.
. Albiński MK, Lutz N, Ceroni D, et al. Paediatric musculoskeletal infections with Panton-Valentine leucocidin. Swiss Med Wkly 2018;148:w14669.
. Gijón M, Bellusci M, Petraitiene B, et al. Factors associated with severity in invasive community-acquired Staphylococcus aureus infections in children: a prospective European multicentre study. Clin Microbiol Infect 2016;22: 643.e1-6.
. Ritz N, Curtis N. The role of Panton-Valentine leukocidin in Staphylococcus aureus musculoskeletal infections in children. Pediatr Infect Dis J 2012;31:514–8.
. David MZ, Daum RS. Community-associated methicillin-resistant Staphylococcus aureus: epidemiology and clinical consequences of an emerging epidemic. Clin Microbiol Rev 2010;23:616–87.
Keywords:Copyright © 2019 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.
bone and joint infections; clindamycin; French Guiana; Panton–Valentine Leukocidin producing Staphylococcus aureus; pericarditis