Origin and significance of Si and O isotope heterogeneities in Phanerozoic, Archean, and Hadean zircon.

Hydrosphere interactions and alteration of the terrestrial crust likely played a critical role in shaping Earth's surface, and in promoting prebiotic reactions leading to life, before 4.03 Ga (the Hadean Eon). The identity of aqueously altered material strongly depends on lithospheric cycling of abundant and water-soluble elements such as Si and O. However, direct constraints that define the character of Hadean sedimentary material are absent because samples from this earliest eon are limited to detrital zircons (ZrSiO4). Here we show that concurrent measurements of Si and O isotope ratios in Phanerozoic and detrital pre-3.0 Ga zircon constrain the composition of aqueously altered precursors incorporated into their source melts. Phanerozoic zircon from (S)edimentary-type rocks contain heterogeneous δ18O and δ30Si values consistent with assimilation of metapelitic material, distinct from the isotopic character of zircon from (I)gneous- and (A)norogenic-type rocks. The δ18O values of detrital Archean zircons are heterogeneous, although yield Si isotope compositions like mantle-derived zircon. Hadean crystals yield elevated δ18O values (vs. mantle zircon) and δ30Si values span almost the entire range observed for Phanerozoic samples. Coupled Si and O isotope data represent a constraint on Hadean weathering and sedimentary input into felsic melts including remelting of amphibolites possibly of basaltic origin, and fractional addition of chemical sediments, such as cherts and/or banded iron formations (BIFs) into source melts. That such sedimentary deposits were extensive enough to change the chemical signature of intracrustal melts suggests they may have been a suitable niche for (pre)biotic chemistry as early as 4.1 Ga.

Legionella bozemanii pulmonary abscess in a pediatric allogeneic stem cell transplant recipient.

Legionella spp. infections are often considered in the differential diagnosis of pneumonia in adults. This case report describes a pediatric stem cell transplant recipient presenting with cavitary pulmonary disease secondary to Legionella bozemanii infection. Also highlighted with this atypical clinical presentation are challenges in diagnosing legionellosis and concerns of increased vulnerability for such infections when severely immunocompromised patients are changed to nontrimethoprim-sulfamethoxazole Pneumocystis jiroveci pneumonia prophylaxis.

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.

Quinupristin-dalfopristin nonsusceptibility in pneumococci from sickle cell disease patients.

Sickle cell disease (SCD) is a risk factor for fatal pneumococcal infection. Nonsusceptibilty to quinupristin-dalfopristin (Q-D) was absent from 105 non-SCD-associated pneumococcal isolates but was present in 33/148 (22%) SCD-associated isolates. One-third of the isolates harbored a known resistance mechanism. Q-D is not optimal for use for the treatment of pneumococcal infection in SCD patients.

Cephalosporin-resistant pneumococci and sickle cell disease.

Sickle cell anemia patients have 600 times the risk for invasive pneumococcal disease than their healthy peers. High-level cephalosporin resistance was described in the 1990s in healthy children from Tennessee, but its prevalence in sickle cell disease patients is unknown. Pneumococcal isolates from sickle cell disease patients from Tennessee were subjected to multilocus sequence typing to characterize antimicrobial drug-resistant strains. Twenty-one percent of strains were resistant to cefotaxime and penicillin. Of the 14 cephalosporin-resistant strains, 9 were sequence types previously described as highly cephalosporin resistant, while resistance was found for the first time in 3 clones: Maryland6B, ST660, and a novel clone, ST1753. High-level cephalosporin resistance exists in more settings than initially recognized, and its high prevalence in sickle cell disease patients may decrease the efficacy of third-generation cephalosporins in invasive pneumococcal disease.

Incidence and etiologies of complicated parapneumonic effusions in children, 1996 to 2001.

BACKGROUND: The incidence and causative organisms associated with complicated parapneumonic effusions in children with community-acquired pneumonia are likely to have changed during the past several years. METHODS: Data regarding clinical and laboratory features were abstracted retrospectively from medical records of 76 subjects with complicated parapneumonic effusions at a tertiary children's hospital from 1996 through 2001. Incidence rates per 10 000 hospital discharges and per 1000 patients with nonviral pneumonia were calculated. RESULTS: Etiologic organisms were Streptococcus pneumoniae (31 subjects), Staphylococcus aureus (7), Streptococcus pyogenes (5), Abiotrophia sp. (1) and no culture-confirmed agent (32). The annual incidence of complicated parapneumonic effusions per 10 000 discharges progressively increased from 4.5 in 1996 to 25.0 in 1999 (P = 0.0001), then declined to 10.1 in 2001 (P = 0.03). Similarly the incidence per 1000 cases of nonviral pneumonia increased from 2.9 in 1996 to 11.0 in 1999 (P = 0.003) and then declined to 4.8 in 2001 (P = 0.053). Whereas S. pneumoniae was the leading confirmed etiology in each year, the proportion of cases caused by Staphylococcus aureus increased from 6% in 1996 to 2000 (all of which were methicillin-susceptible) to 30% in 2001 (all methicillin-resistant; P = 0.04). CONCLUSIONS: The incidence of complicated parapneumonic effusions in children with community-acquired pneumonia increased from 1996 to 1999 and then declined concomitant with the introduction of the pneumococcal conjugate vaccine. Although cases caused by S. pneumoniae have decreased, community onset methicillin-resistant Staphylococcus aureus has emerged as a cause of pneumonia with complicated effusions in children.