Nosocomial outbreak of Clostridium difficile-associated diarrhoea due to a clindamycin-resistant enterotoxin A-negative strain.

A clindamycin-resistant toxin A-negative, toxin B-positive Clostridium difficile strain caused an outbreak among 24 hospitalized patients at the Department of Surgery, the Intensive Care unit, and the Department of Internal Medicine of an 800-bed academic hospital. Nineteen patients had undergone a surgical intervention and all 24 patients received at least one dose of antibiotics prior to the development of Clostridium difficile-associated diarrhoea. Twenty-seven episodes of Clostridium difficile-associated diarrhoea in 24 patients were categorized as mild (n=19), severe (n=7), or fatal (n=1). Relapses occurred in three patients. Nineteen of the 27 episodes required anti-Clostridium difficile treatment. Molecular typing performed by arbitrary primer polymerase chain reaction (PCR) and PCR amplification of rRNA intergenic spacer regions revealed that the outbreak strains recovered from culture were identical. The outbreak strain belonged to serogroup F and was resistant to erythromycin, clindamycin, and tetracycline, whereas susceptibility to chloramphenicol varied. No phenotypic activity of enterotoxin A was detected. A deletion of approximately 1.7 kb was found in the toxin A gene. Cytotoxin B had an unusual effect on cell culture assays that, at first, was not recognized as Clostridium difficile specific but could be neutralized with anti-Clostridium difficile B cytotoxin.

Decreased lung function associated with perinatal exposure to Dutch background levels of dioxins.

UNLABELLED: Perinatal exposure to Dutch background dioxin levels is rather high. Studies of calamities have shown that dioxins negatively influence the respiratory system. It was hypothesized that perinatal exposure to background dioxin levels leads to lung suboptimality, probably through developmental interference. This study aimed to assess lung function in relation to perinatal dioxin exposure. Spirometry was performed in 41 healthy children (aged 7-12 y. mean 8.2 y) with known perinatal dioxin exposure. The ratio of forced expiratory volume in I s to forced vital capacity (FEV1/FVC ratio) was determined. A complete medical history was taken. The prenatal exposure ranged from 8.74 to 88.8 (mean 34.6) ng TEQ dioxin kg fat(-1), measured in breast milk. The postnatal exposure ranged from 4.34 to 384.51 (mean 75.4) ng TEQ dioxin. Twelve children had to be excluded. A significant decrease in lung function in relation to both prenatal (p = 0.045) and postnatal (p = 0.0002) dioxin exposure was seen in the 29 non-excluded children. A clinical association between chest congestion and perinatal dioxin exposure was seen. CONCLUSION: Perinatal background dioxin exposure may be inversely associated with the FEV1/ FVC ratio.

Humoral changes during and following coronary bypass surgery: relationship to postoperative blood pressure.

In this study we investigated the role of the renin-angiotensin system and the adrenergic system in the hypertensive response during and following coronary bypass surgery. Arterial blood samples for measurement of active renin, angiotensin II, aldosterone and catecholamines were drawn before, during and in the first period after coronary artery grafting. Both noradrenaline and adrenaline rose significantly during extracorporeal circulation and remained elevated afterwards, the rise in adrenaline preceding that of noradrenaline. During cardiopulmonary bypass renin also increased while angiotensin II increased after an initial fall. Postoperatively, renin tended to return to control levels. However, angiotensin II fell in some patients but remained elevated in others. The latter group had significantly lower blood pressure during cardiopulmonary bypass, but higher pressure thereafter. Aldosterone levels were markedly reduced during cardiopulmonary bypass. The results suggest that low pressure during extracorporeal circulation may trigger enhanced formation of angiotensin II, apparently involving extrapulmonary converting enzyme. This mechanism may, when acting in concert with an activated sympathetic nervous system, produce significant blood pressure elevation postoperatively.