Aims

We aimed to describe the epidemiological, biological, and bacteriological characteristics of osteoarticular infections (OAIs) caused by Kingella kingae.

Aim. Differentiation between bone infarction and bone infection in sickle cell disease has traditionally been difficult, even with modern imaging techniques, and widespread antibiotic use is common. Early differentiation between the two conditions would enable more appropriate targeting of radiological investigations, antibiotics and surgery, and avoid un-necessary antibiotic usage. Method. At our tertiary paediatric sickle cell centre, we have developed a sequencing protocol to be able to accurately differentiate between infection and infarction in sickle cell children using Magnetic Resonance (MR) Imaging. We have undertaken a preliminary retrospective study to analyse clinical and laboratory parameters in these children to see whether earlier differentiation prior to MR imaging is possible. Results. We identified 52 episodes in 27 patients of bony pain in sickle cell children between 2006 and 2012. In 30 episodes in 27 patients, the MR sequences used allowed accurate determination of pathology, diagnosing infarction in 19 episodes in 17 patients, and infection in 8 episodes in 7 patients. The remainder showed no evidence of acute infarction or infection despite pain. As a general trend, admission white cell counts were higher in the infection group, with a temperature on admission also being more likely. There was no significant difference in CRP or platelet count between the infarction and infection groups. Conclusion. From a small retrospective study it may be possible to identify factors making infection as a cause of bone pain in sickle cell disease more likely, enabling better targeting of urgent MR imaging and surgery and preventing un-necessary antibiotic usage. A larger, prospective study is required and is currently underway

Aims

This multicentre, retrospective study aimed to improve our knowledge of primary pyogenic spinal infections in children by analyzing a large consecutive case series.

The role of heritable thrombophilic risk factors in the pathogenesis of the Perthes’ disease is controversial. The clinical and radiological findings of Perthes’ disease may be indistinguishable from those of Gaucher’s disease, and the most common Jewish N370S Gaucher mutation is threefold greater in patients with Perthes’ disease. Familial osteonecrosis of the femoral head is associated with variant mutations of collagen type II (COL2A1 mutations). We therefore studied the potential role of genetic thrombophilia and the Gaucher and COL2A1 mutations in children with Perthes’ disease.

Genomic DNA of 119 children with radiologically-confirmed Perthes’ disease diagnosed between 1986 and 2005 was analysed for the thrombophilic polymorphisms Factor V Leiden, 677T-MTHFR and FIIG20210A. The results were compared with those of a group of 276 children without Perthes’ disease. DNA was also analysed for the Gaucher mutations N370S, G insertion (84GG), L444P, Intron 2 (IVS2+1G> A) and R496H. Enzymic assays confirmed the Gaucher disease status. Collagen (COL2A1) mutations of the 12q13 gene were also analysed. The prevalence of thrombophilic markers was similar among the 119 patients with Perthes’ disease and the 276 control subjects. The prevalence of the Gaucher mutation was consistent with Israeli population carriership data and did not confirm an earlier-claimed association with Perthes’ disease. All 199 patients were negative for the studied COL2A1 mutations.

We found no genetic association between Perthes’ disease and either Gaucher’s disease or COL2A1 mutations or increased genetic thrombophilia among our patients compared with the control group. A systematic review of case-control studies suggested that there was a positive association between Perthes’ disease and Factor V Leiden. The impact of this association upon the disease, although not consistent across the studies, remains unclear.

Between September 2004 and December 2005 we carried out a prospective study of all cases of sepsis of the hip in childhood at a South African regional hospital with a large local population, and which also took referrals from nine rural hospitals. The clinical, radiological, ultrasound and bacteriological features were assessed. All the hips were drained by arthrotomy and the diagnosis was confirmed microbiologically and histologically. Hips with tuberculosis were excluded. The children were reviewed in a dedicated clinic at a mean follow-up of 8.1 months (3 to 18).

There were 40 hips with sepsis in 38 patients. Two patients were lost to follow-up. Nine (24%) had multi-focal sepsis. Overall, 13 hips (34%) had a full and uncomplicated clinical and radiological recovery and 25 (66%) had complications. All patients treated by arthrotomy and appropriate antibiotics within five days of the onset of symptoms had an uncomplicated recovery. Initial misdiagnosis was associated with a delay to arthrotomy. However, ‘deprivation’, consultation with a traditional healer, maternal educational attainment and distance to a primary health-care facility were not associated with delay to arthrotomy. The early correct diagnosis of this condition, common in the developing world, remains a significant factor in improving the clinical outcome.