Burkholderia cepacia is a ubiquitous, opportunistic, environmental gram-negative bacillus which most commonly affects cystic fibrosis and immunocompromised patients. Rarely, it can cause peritoneal dialysis (PD) exit-site infection (ESI). Information relating to predisposing factors, clinical course, and treatment options for B. cepacia ESIs is limited. Although reports of B. cepacia healthcare-associated infections exist, outbreaks in PD units have not previously been reported. A recent outbreak of B. cepacia ESI in our PD unit provided a unique opportunity to study B. cepacia ESIs and to outline an approach to investigating such an outbreak. After unexpectedly identifying B. cepacia as the cause of PD catheter ESIs in 3 patients over an 11-week period, we began systematically screening our PD population for B. cepacia exit-site colonization. A further 6 patients were found to be affected, 3 with asymptomatic colonization and 3 with symptomatic B. cepacia ESI. Four of the 6 developed tunnel infections requiring multiple courses of antibiotic treatment, and 3 patients required catheter removal; 2 patients with symptomatic ESIs without tunnel involvement responded to oral and topical antibiotics. Further investigation implicated 4% chlorhexidine aqueous bodywash used by all patients as the probable source of the outbreak. This is the first reported outbreak of B. cepacia ESIs. We noted an association between diabetes mellitus and refractory/more extensive infection. Our experience suggests that isolated ESIs can be treated successfully with oral antibiotics whereas tunnel infections generally require catheter removal.
evidence presented here that the anodal component of Hp 2-1 contains only 8 and al chains makes its identity with the Hp 1-1 of the corresponding al type very likely. It would be of interest to extend these studies to the polymer bands of the rare phenotypes Hp 2-1M10 and Hp "Johnson.""1 It seems reasonable to assume that the assembly of the various chains of Hp to form the Hp 2-1 polymers occurs very soon after the chains are synthesized since artificial mixtures of Hp 2-2 and Hp 1-1, even after prolonged incubation, show no tendency to form 2-1 polymers.'2 The mechanism of this assembly is unknown. Summary.-Polymer bands of Hp 2-1, freed from the anodal component by gel filtration, are shown to contain appreciable amounts of a1 chains which are characteristic of Hp 1-1. This is taken as evidence in support of Allison's hypothesis that the polymers of Hp 2-1 differ from those of Hp 2-2 in containing Hp' gene products as an integral part of their structure. The anodal component of Hp 2-1 is shown to resemble Hp 1-1 in its chain composition. The author wishes to thank Miss Elaine Henry for technical assistance.
Our previous investigations have indicated that ‘let-down’ sensation in the mammary gland in nursing, or on injection of Pituitrin, is accompanied by slow electric response. This was believed to emanate from secreting-gland cells or from contractile myoepithelial cells. Indirect control indicated that sweat-gland activity, related to emotional reaction, played little part in electric response recorded from the breast. We have controlled this question of sweat-gland participation in observed response by recording simultaneously from the palm of the hand and from the areola in a non-lactating subject. It was found that spoken words evoking emotional reactions were accompanied by large electric responses from the palm, but from the areola there were either no responses or very small inverse deflections, presumably due to sweat glands in the skin of the thorax. Observations on lactating subjects showed that during nursing occasional deflections in the palmar record resembled those evoked in word tests, but in no case did the palmar record show a slow response synchronized with that recorded from the areola during the letdown. From these observations we conclude that sweat-gland reactions play little part in the characteristic let-down electric response led off from the areola. This must arise from a different source, presumably either the myoepithelial cells, the secreting cells, or both. Submitted on January 14, 1960
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