Early onset infection (EOI) in preterm infants <32 weeks gestational age (GA) is associated with a high mortality rate and the development of severe acute and long-term complications. The pathophysiology of EOI is not fully understood and clinical and laboratory signs of early onset infections in this patient cohort are often not conclusive. Thus, the aim of this study was to identify signatures characterizing preterm infants with EOI by using genome-wide gene expression (GWGE) analyses from umbilical arterial blood of preterm infants. This prospective cohort study was conducted in preterm infants <32 weeks GA. GWGE analyses using CodeLink human microarrays were performed from umbilical arterial blood of preterm infants with and without EOI. GWGE analyses revealed differential expression of 292 genes in preterm infants with EOI as compared to infants without EOI. Infants with EOI could be further differentiated into two subclasses and were distinguished by the magnitude of the expression of genes involved in both neutrophil and T cell activation. A hallmark activity for both subclasses of EOI was a common suppression of genes involved in natural killer (NK) cell function, which was independent from NK cell numbers. Significant results were recapitulated in an independent validation cohort. Gene expression profiling may enable early and more precise diagnosis of EOI in preterm infants.Key message Gene expression (GE) profiling at birth characterizes preterm infants with EOI.GE analysis indicates dysregulation of NK cell activity.NK cell activity at birth may be a useful marker to improve early diagnosis of EOI. Electronic supplementary materialThe online version of this article (doi:10.1007/s00109-016-1466-4) contains supplementary material, which is available to authorized users.

A 28-year-old previously healthy woman in the third trimester of pregnancy presented with hemoptysis ("mouth repeatedly full of blood"). Bronchoscopy showed diffuse right bronchial bleeding associated with transient gas-exchange disorder. Clinical examination revealed a low likelihood of pulmonary embolism, duplex sonography of the leg veins was negative, and echocardiography showed no abnormalities. Despite the patient's pregnancy we carried out contrast-enhanced thoracic computed tomography to detect, for example, any pulmonary vascular malformation. A shunt between the right bronchial artery and the pulmonary vein, visualized due to suboptimal contrast enhancement, was treated with catheter-assisted coiling. The bleeding ceased, and 10 weeks later the patient gave birth to a healthy girl. Rupture of a pulmonary arteriovenous malformation (PAVM) is a life-threatening event that occurs more frequently during pregnancy. Hormone-induced angiogenesis has been proposed as a possible cause. There have been only few reports of PAVMs from bronchial arteries. In our patient the malformation would probably have gone undetected if the contrast enhancement had not been inadequate. Because of its exposure to contrast medium, the newborn child should undergo thyroid function testing.

No abstract

No abstract

An underweight 65-year-old man was admitted to the hospital for evaluation of lower abdominal pain. Computed tomography (CT) of the abdomen revealed a small amount of ascites, peritoneal contrast enhancement, and multiple mesenteric nodules, arousing the suspicion of peritoneal carcinomatosis. An enzyme-linked immunospot assay (ELSIPOT) for mycobacterium-tuberculosis-specific T-cells was positive. Specimens of ascitic fluid and peritoneal membrane were obtained by laparoscopy. Histological examination revealed numerous epithelioid-cell granulomata, and bacterial culture confirmed the diagnosis of peritoneal tuberculosis due to Mycobacterium caprae. M. caprae causes tuberculosis in ungulates (e.g., cows, deer) and is found in the Alpine regions and elsewhere. This zoonosis can spread to man through occupational exposure (cattle farming) or through the drinking of unpasteurized milk. Our patient was asymptomatic after a classic six-month course of antitubercular therapy. His mechanism of exposure was never conclusively determined.