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PubMed2001

Lethal pneumococcal infection in an 18-month-old girl with splenic hypoplasia and dysgammaglobulinemia.

We report the case of an 18-month-old girl who died of overwhelming pneumococcal sepsis. Autopsy revealed a small spleen with unusual architecture. There was a marked rarefaction of the white pulp with only very few but florid germinal centers. Immunohistochemical staining showed a low number of T and B lymphocytes in the spleen, whereas normal numbers and distribution of lymphocytes were found in all other primary and secondary lymphatic organs. Whereas levels of IgM were normal, IgA and IgG levels were significantly lower than in age-matched controls. Consistent with serological data, B cells mainly expressed IgM and IgD, whereas IgG expression was lower than expected. Additionally, intestinal immunoglobulin distribution in B-cell areas of lymphofollicular hyperplasia showed normal expression of IgM, but almost no expression of IgA. A review of the literature failed to disclose a similar case of dysgammaglobulinemia associated with isolated structural spleen anomalies. We propose that the patient suffered from a defect of the B-cell differentiation pathway.

Dysgammaglobulinemia↗
PubMed1999

Spleen sizing by ultrasound scan and risk of pneumococcal infection in patients with chronic GVHD: preliminary observations.

Encapsulated bacteria infections (EBI) can cause severe complications after BMT, usually occurring in patients with chronic GVHD (cGVHD) and attributed to functional hyposplenism. Using ultrasound (US) scan, we measured spleen size in 22 patients transplanted from HLA identical siblings, with or without cGVHD. No patient had received TBI, spleen irradiation or penicillin prophylaxis. Results were correlated with occurrence of EBI during a mean follow-up of 55 months (range 7-93). In the group without cGVHD, the difference between pre- and post-BMT spleen longitudinal diameters was not significant, and no patient developed EBI. In the cGVHD group, post-BMT spleen longitudinal diameters were significantly smaller than those pre-BMT (9.1+/-1.6 vs. 12.3+/-2.2; P = 0.0005). Out of four patients with cGVHD who showed a major spleen size reduction, two developed a severe infection (an overwhelming sepsis and a pneumococcal meningitis). In our small series, we found a borderline relationship between spleen size reduction and duration of cGVHD (P = 0.06), as well as an increased risk of life-threatening infection in patients with extensive cGVHD and hyposplenism as detected by US scan. We conclude that US scan may be useful to detect spleen size reduction following allogeneic BMT and that penicillin prophylaxis is to be strongly recommended in patients with extensive cGVHD and spleen size reduction, even in those who have not received total body or spleen irradiation.

Adult↗
PubMed2001

Invasive pneumococcal infection and drug-resistant Streptococcus pneumoniae in Thai children.

Sixty-eight children with systemic Streptococcus pneumoniae infection were identified by hospital chart review between 1986-1997. The age distribution varied from 2 days to 15 years, with a mean age of 3.3 years. There were 35 boys and 33 girls. Four clinical entities included 30 cases of meningitis, 20 cases of pneumonia, 10 cases of peritonitis and 8 cases of septicemia/bacteremia. Forty patients (58.8%) had underlying diseases. Seventeen patients (25.0%) developed early complications and the mortality rate was 8.8 per cent. The percentage of susceptible isolates to penicillin, chloramphenicol, cefotaxime/ceftriaxone, ciprofloxacin, imipenem and vancomycin were 69.6, 91.3, 100.0, 87.2, 100.0 and 97.1 per cent, respectively. There were six cases of drug-resistant S. pneumoniae (DRSP) infection; 3 cases of meningitis, one case of pneumonia, one case of infective endocarditis and one case of purpura fulminans. Our data indicate that S. pneumoniae infection is relatively serious and life-threatening. There is a trend of increasing prevalence of invasive pneumococcal and DRSP infections.

Adolescent↗
PubMed2007

Hypersusceptibility to invasive pneumococcal infection in experimental sickle cell disease involves platelet-activating factor receptor.

Children with sickle cell disease have a 600-fold increased incidence of invasive pneumococcal disease. Platelet-activating factor receptor (PAFr) mediates pneumococcal invasion, and up-regulation of PAFr on chronically activated endothelia could contribute to increased bacterial invasion. Mice transplanted with sickle cell bone marrow developed more extensive infection, and 57% died, compared with 16% of wild-type mice. Histopathological analysis revealed that sickle cell mice expressed significantly more PAFr on endothelia and epithelia. Pharmacological blockade or genetic deletion of PAFr protected sickle cell mice from mortality. We conclude that PAFr plays an important role in hypersusceptibility to pneumococcal infection in sickle cell disease.

Anemia, Sickle Cell↗