The possible causative agent of childhood community-acquired pneumonia can be detected in most cases. Further studies are warranted to determine what etiologic investigations would aid in the management of pneumonia. With effective immunization for S. pneumoniae and respiratory syncytial virus infections, more than one-half of the pneumonia cases in this study could have been prevented.

Bordetella pertussis causes pertussis, a respiratory disease that is most severe for infants. Vaccination was introduced in the 1950s, and in recent years, a resurgence of disease was observed worldwide, with significant mortality in infants. Possible causes for this include the switch from whole-cell vaccines (WCVs) to less effective acellular vaccines (ACVs), waning immunity, and pathogen adaptation. Pathogen adaptation is suggested by antigenic divergence between vaccine strains and circulating strains and by the emergence of strains with increased pertussis toxin production. We applied comparative genomics to a worldwide collection of 343 B. pertussis strains isolated between 1920 and 2010. The global phylogeny showed two deep branches; the largest of these contained 98% of all strains, and its expansion correlated temporally with the first descriptions of pertussis outbreaks in Europe in the 16th century. We found little evidence of recent geographical clustering of the strains within this lineage, suggesting rapid strain flow between countries. We observed that changes in genes encoding proteins implicated in protective immunity that are included in ACVs occurred after the introduction of WCVs but before the switch to ACVs. Furthermore, our analyses consistently suggested that virulence-associated genes and genes coding for surface-exposed proteins were involved in adaptation. However, many of the putative adaptive loci identified have a physiological role, and further studies of these loci may reveal less obvious ways in which B. pertussis and the host interact. This work provides insight into ways in which pathogens may adapt to vaccination and suggests ways to improve pertussis vaccines.

A more virulent strain of the disease is emerging.

Background: A study was undertaken to investigate the differential diagnostic role of chest radiographic findings, total white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and serum C reactive protein (CRP) in children with community acquired pneumonia of varying aetiology. Methods: The study population consisted of 254 consecutive children admitted to hospital with community acquired pneumonia diagnosed between 1993 and 1995. WBC, ESR, and CRP levels were determined on admission. Seventeen infective agents (10 viruses and seven bacteria) were searched for. Chest radiographs were retrospectively and separately reviewed by three paediatric radiologists. Results: A potential causative agent was found in 215 (85%) of the 254 cases. Bacterial infection was found in 71% of 137 children with alveolar infiltrates on the chest radiograph, while 72% of the 134 cases with a bacterial pneumonia had alveolar infiltrates. Half of the 77 children with solely interstitial infiltrates on the chest radiograph had evidence of bacterial infection. The proportion of patients with increased WBC or ESR did not differ between bacterial and viral pneumonias, but differences in the CRP levels of >40 mg/l, >80 mg/l, and >120 mg/l were significant although the sensitivity for detecting bacterial pneumonia was too low for use in clinical practice. Conclusions: Most children with alveolar pneumonia, especially those with lobar infiltrates, have laboratory evidence of a bacterial infection. Interstitial infiltrates are seen in both viral and bacterial pneumonias.

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The results indicate that the measurement of serum PCT, CRP and IL-6 has little value in the differentiation of bacterial and viral pneumonia in children. However, in some patients with very high serum PCT, CRP or IL-6 values, bacterial pneumonia is probable.

SummaryAlthough previous studies using human cytokines in rabbits and rats have provided evidence ofthe participation oftumor necrosis factor a (TNF-(x) and interleukin lß (IL1ß) in the meningeal inflammatory cascade, the results obtained by several groups ofinvestigators have been discordant or, at times, contradictory. In the present study, homologous cytokines were applied to the rabbit meningitis model. Intracisternal administration of 102-10 1 IU of purified rabbit TNF-a (RaTNF-a) produced significant cerebrospinal fluid (CSF) inflammation. A similar response was observed after intracisternal inoculation of 5-200 ng of rabbit recombinant ILlß (rrIL1ß) . Preincubation of these two mediators with their specific antibodies resulted in an almost complete suppression of the CSF inflammatory response. In animals with Haemophilus influenzae type b lipooligosaccharide-induced meningitis, intracisternal administration of anti-rrlIrlß, anti-RaTNF-a, or both resulted in a significant modulation of meningeal inflammation. Simultaneous administration of 103 IU of RaTNF-a and 5 ng of rrILlß resulted in a synergistic inflammatory response manifested by a more rapid and significantly increased influx of white blood cells into the CSF compared with results after each cytokine given alone. These data provide evidence for a seminal role of TNF-a and IL1ß in the initial events of meningeal inflammation.

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