Meningococcal bacterial DNA load at presentation correlates with disease severity. Issue 1 (1st January 2002)

• Record Type: Journal Article
• Authors: Hackett, S J; Guiver, M; Marsh, J; Sills, J A; Thomson, A P J; Kaczmarski, E B; Hart, C A
• Is Part Of: Archives of disease in childhood. Volume 86:Issue 1(2002)
• Page Start: 44
• Page End: 46
• Publication Date: 2002-01-01
• Subjects: meningococcal disease -- bacterial load -- disease severity; Children -- Diseases -- Periodicals; Infants -- Diseases -- Periodicals; 618.920005
• DOI: 10.1136/adc.86.1.44
• Languages: English
• ISSNs: 0003-9888

Abstract

Abstract : Aims: To determine bacterial loads in meningococcal disease (MCD), their relation with disease severity, and the factors which determine bacterial load. Methods: Meningococcal DNA quantification was performed by the Taqman PCR method on admission and sequential blood samples from patients with MCD. Disease severity was assessed using the Glasgow Septicaemia Prognostic Score (GMSPS, range 0–15, severe disease ≥8). Results: Median admission bacterial load was 1.6 × 10 6 DNA copies/ml of blood (range 2.2 × 10 4 to 1.6 × 10 8 ). Bacterial load was significantly higher in patients with severe (8.4 × 10 6 ) compared to milder disease (1.1 × 10 6, p = 0.018). This difference was greater in septicaemic patients (median 1.6 × 10 7 versus 9.2 × 10 5, p < 0.001). Bacterial loads were significantly higher in patients that died (p = 0.017). Admission bacterial load was independent of the duration of clinical symptoms prior to admission, with no difference between the duration of symptoms in mild or severe cases (median, 10.5 and 11 hours respectively). Bacterial loads were independent of DNA elimination rates following treatment. Conclusion: Patients with MCD have higher bacterial loads than previously determined with quantitative culture methods. Admission bacterial load is significantly higher in patients with severe disease (GMSPS ≥8) and maximum load is highest in those who die. Bacterial load is independent of the duration of clinical symptoms or the decline in DNA load.