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Invasive pneumococcal infections in children infected with HIV are not associated with splenic dysfunction
W A Andiman1, J Simpson, C Holtkamp
1Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut, USA.
Insights
Splenic dysfunction does not explain the higher rates of invasive pneumococcal disease in children with HIV. Pocked red blood cell counts were normal in HIV-infected children, even those with infections.
Area of Science:
- Pediatric Infectious Diseases
- Immunology
- Hematology
Background:
- Children with human immunodeficiency virus (HIV) have an increased risk of invasive bacterial infections.
- Encapsulated bacteria, such as Streptococcus pneumoniae, are common pathogens in this population.
- Splenic dysfunction is a known risk factor for invasive pneumococcal disease.
Purpose of the Study:
- To determine if splenic dysfunction, assessed by pocked red blood cell (RBC) counts, contributes to the increased incidence of invasive pneumococcal disease in HIV-infected children.
- To evaluate the relationship between splenic reticuloendothelial function and pneumococcal infections in pediatric HIV.
Main Methods:
- Assessed splenic reticuloendothelial function in 84 children (70 HIV-infected, 14 controls) using phase interference microscopy to count pocked RBCs.
- Reviewed medical records and a microbiology database for diagnoses of invasive bacterial infections.
- Correlated splenic function markers with the occurrence of invasive pneumococcal disease.
Main Results:
- All 84 children had normal proportions of pocked RBCs (< 2%), including those who developed invasive pneumococcal disease.
- Seventeen of 70 HIV-infected children experienced 23 invasive bacterial infections, all caused by Streptococcus pneumoniae.
- No invasive bacterial infections occurred in the control group or in the majority of HIV-infected children.
Conclusions:
- Splenic dysfunction, as indicated by pocked RBC counts, does not appear to be the primary driver of increased invasive pneumococcal disease in HIV-infected children.
- The findings suggest other mechanisms contribute to the heightened susceptibility to pneumococcal infections in this cohort.
Objectives:
Children infected with HIV-1 are more likely to acquire infections associated with the encapsulated bacterial pathogens of childhood than their non-HIV-infected peers. The goal of the current study was to determine what proportion of community-acquired, invasive pneumococcal disease in HIV-infected children could be attributed to splenic dysfunction, as measured by enumerating the number of pocked red blood cells (RBCs) in peripheral blood.
Methods:
Splenic reticuloendothelial function was assessed semiquantitatively by examining the morphology of the RBCs of 84 children born to HIV-infected mothers using phase interference microscopy. Surveillance of medical records, and a review of the Yale-New Haven Hospital Clinical Microbiology computerized database, revealed that all of the bacterial cultures of blood and cerebrospinal fluid from these patients were positive.
Results:
Of the 84 children assessed, 70 were infected with HIV (median age 66 months) and 14 were uninfected seroreverters (controls). Sixty-one of the 70 HIV-infected children met the CDC criteria for moderate or severe immunodeficiency and/or moderate or severe symptomatic conditions. Seventeen of the 70 HIV-infected children experienced 23 invasive bacterial infections. Streptococcus pneumoniae was responsible for all 23 infections. The median age at the time of first infection among these 17 subjects was 20 months (range, 10-58 months). There were no episodes of invasive bacterial infections in the remaining 53 HIV-infected children nor among the 14 controls. All 84 children studied, including those with invasive pneumococcal disease, had normal proportions (i.e., < 2%) of pocked erythrocytes in peripheral blood.
Conclusion:
Splenic dysfunction, as measured by the pocked RBC count, does not account for the increased occurrence of invasive pneumococcal disease found in children infected with HIV.