[Guidelines for the Management of Community Acquired Pneumonia in Children and Adolescents (Pediatric Community Acquired Pneumonia, pCAP) - Issued under the Responsibility of the German Society for Pediatric Infectious Diseases (DGPI) and the German Society for Pediatric Pulmonology (GPP)]. / S2k-Leitlinie Management der ambulant erworbenen Pneumonie bei Kindern und Jugendlichen (pädiatrische ambulant erworbene Pneumonie, pCAP).

The present guideline aims to improve the evidence-based management of children and adolescents with pediatric community-acquired pneumonia (pCAP). Despite a prevalence of approx. 300 cases per 100 000 children per year in Central Europe, mortality is very low. Prevention includes infection control measures and comprehensive immunization. The diagnosis can and should be established clinically by history, physical examination and pulse oximetry, with fever and tachypnea as cardinal features. Additional signs or symptoms such as severely compromised general condition, poor feeding, dehydration, altered consciousness or seizures discriminate subjects with severe pCAP from those with non-severe pCAP. Within an age-dependent spectrum of infectious agents, bacterial etiology cannot be reliably differentiated from viral or mixed infections by currently available biomarkers. Most children and adolescents with non-severe pCAP and oxygen saturation > 92 % can be managed as outpatients without laboratory/microbiology workup or imaging. Anti-infective agents are not generally indicated and can be safely withheld especially in children of young age, with wheeze or other indices suggesting a viral origin. For calculated antibiotic therapy, aminopenicillins are the preferred drug class with comparable efficacy of oral (amoxicillin) and intravenous administration (ampicillin). Follow-up evaluation after 48 - 72 hours is mandatory for the assessment of clinical course, treatment success and potential complications such as parapneumonic pleural effusion or empyema, which may necessitate alternative or add-on therapy.

Phylogenomics of the killer whale indicates ecotype divergence in sympatry.

For many highly mobile species, the marine environment presents few obvious barriers to gene flow. Even so, there is considerable diversity within and among species, referred to by some as the 'marine speciation paradox'. The recent and diverse radiation of delphinid cetaceans (dolphins) represents a good example of this. Delphinids are capable of extensive dispersion and yet many show fine-scale genetic differentiation among populations. Proposed mechanisms include the division and isolation of populations based on habitat dependence and resource specializations, and habitat release or changing dispersal corridors during glacial cycles. Here we use a phylogenomic approach to investigate the origin of differentiated sympatric populations of killer whales (Orcinus orca). Killer whales show strong specialization on prey choice in populations of stable matrifocal social groups (ecotypes), associated with genetic and phenotypic differentiation. Our data suggest evolution in sympatry among populations of resource specialists.

Social cohesion among kin, gene flow without dispersal and the evolution of population genetic structure in the killer whale (Orcinus orca).

In social species, breeding system and gregarious behavior are key factors influencing the evolution of large-scale population genetic structure. The killer whale is a highly social apex predator showing genetic differentiation in sympatry between populations of foraging specialists (ecotypes), and low levels of genetic diversity overall. Our comparative assessments of kinship, parentage and dispersal reveal high levels of kinship within local populations and ongoing male-mediated gene flow among them, including among ecotypes that are maximally divergent within the mtDNA phylogeny. Dispersal from natal populations was rare, implying that gene flow occurs without dispersal, as a result of reproduction during temporary interactions. Discordance between nuclear and mitochondrial phylogenies was consistent with earlier studies suggesting a stochastic basis for the magnitude of mtDNA differentiation between matrilines. Taken together our results show how the killer whale breeding system, coupled with social, dispersal and foraging behaviour, contributes to the evolution of population genetic structure.

Low genetic variation among killer whales (Orcinus orca) in the eastern north Pacific and genetic differentiation between foraging specialists.

Killer whales from the coastal waters off California through Alaska were compared for genetic variation at three nuclear DNA markers and sequenced for a total of 520 bp from the mitochondrial control region. Two putative sympatric populations that range throughout this region were compared. They can be distinguished by social and foraging behavior and are known as "residents" and "transients". We found low levels of variation within populations compared to other cetacean species. Comparisons between fish (resident) versus marine mammal (transient) foraging specialists indicated highly significant genetic differentiation at both nuclear and mitochondrial loci. This differentiation is at a level consistent with intraspecific variation. A comparison between two parapatric resident populations showed a small but fixed mtDNA haplotype difference. Together these data suggest low levels of genetic dispersal between foraging specialists and a pattern of genetic differentiation consistent with matrifocal population structure and small effective population size.

[Congenital diaphragmatic hernia--results of an ECMO-centre]. / Angeborene Zwerchfellhernie -Ergebnisse eines ECMO-Zentrums.

BACKGROUND: In recent years increasing survival rates of neonates with congenital diaphragmatic hernia were reported. We present the results of our collective with regard to outcome and predictors of prognosis (need for ECMO, survival). PATIENTS AND METHODS: The neonates with congenital diaphragmatic hernia treated between December 1997 and June 2001 in the university children's hospital Mannheim were included. All patients with congenital diaphragmatic hernia were treated by a defined algorithm including prenatal pulmonary maturation, surfactant immediately after birth, ""gentle ventilation"", inhaled NO, high frequency ventilation and, if necessary, ECMO. We looked at early predictors of the clinical course, e. g. need for ECMO and survival: Birth weight, oxygenation index, ventilation index, the highest and the lowest arterial oxygen and the lowest carbon dioxide partial pressures during the first 24 hours in the ECMO-centre. RESULTS: Between December 1997 and June 2001 50 neonates with congenital diaphragmatic hernia were treated (24 inborn, all of them diagnosed prenatally, 26 transferred after birth). Mean OI was 45.5 cmH2O/mmHg (no ECMO: 16.4 cmH2O/mmHg; ECMO: 62.1 cmH2O/mmHg) mean VI was 133.8 cmH2O x mmHg (no ECMO: 83.9 cmH2O x mmHg; ECMO: 156.2 cmH2O x mmHg). The survival rate was 84 %. According to our algorithm 50% of the patients were treated with ECMO, 78% of the patients treated with ECMO survived. 3 Patients were excluded by the therapy option ECMO, because of contraindications. If the patients need to be treated with ECMO, the predictors of prognosis do not allow to draw conclusions on the clinical course regarding the survival of the patients. CONCLUSION: Our algorithm allows a good survival rate in patients with congenital diaphragmatic hernia. CDH patients seem to have a benefit from transfer into an ECMO centre as early as possible or prenatally. There is no basis according our experiences to exclude patients with congenital diaphragmatic hernia from ECMO. To evaluate the predictors of prognosis regarding the question, which patients do not require ECMO, which patients have a benefit of ecmo, and which patients will die despite ecmo a nationwide cdh-register could be helpful.