Driveline erosion of the colon as a late complication of LVAD implantation.

A 69-year-old man with ischemic cardiomyopathy underwent left ventricular assist device (LVAD) implantation as destination therapy. One month after LVAD placement, the patient reported abdominal pain with driveline site purulence. Serial wound and blood cultures were positive for various Gram-positive and Gram-negative organisms. Abdominal imaging revealed a possible intracolonic course of the driveline at the splenic flexure, but there were no imaging findings suggestive of bowel perforation. A colonoscopy did not identify a perforation. The patient was treated with antibiotics but continued to experience driveline infections over the next 9 months until frank stool started draining from the driveline exit site. Our case illustrates driveline erosion of the colon causing the insidious formation of an enterocutaneous fistula and highlights a rare late complication of LVAD therapy. Learning objective: Colonic erosion by the driveline can cause enterocutaneous fistula formation over a period of months. A change from typical infectious organisms for driveline infection should prompt investigation of a gastrointestinal source. In cases where computed tomography of the abdomen does not show perforation and there is concern for an intracolonic course of the driveline, colonoscopy or laparoscopy may be diagnostic.

Bacterial turgor pressure can be measured by atomic force microscopy.

We report a study of the deformability of a bacterial wall with an atomic force microscope (AFM). A theoretical expression is derived for the force exerted by the wall on the cantilever as a function of the depths of indentation generated by the AFM tip. Evidence is provided that this reaction force is a measure for the turgor pressure of the bacterium. The method was applied to magnetotactic bacteria of the species Magnetospirillum gryphiswaldense. Force curves were generated on the substrate and on the bacteria while scanning laterally. With the mechanical properties so gained we obtained the spring constant of the bacterium as a whole. Making use of our theoretical results we determined the turgor pressure to be in the range of 85 to 150 kPa.

Redox properties of iron in the binding site(s) of F1ATPase from mammalian mitochondria and thermophilic bacterium PS3: a comparative study.

Iron ions in the two iron centers of beef heart mitochondrial F1ATPase, which we have been recently characterized (FEBS Letters 1996, 379, 231-235), exhibit different redox properties. In fact, the ATP-dependent site is able to maintain iron in the redox state of Fe(II) even in the absence of reducing agents, whereas in the nucleotide-independent site iron is oxidized to Fe(III) upon removal of the reductant. Fe(III) ions in the two sites display different reactivity towards H2O2, because only Fe(III) bound in the nucleotide-independent site rapidly reacts with H2O2 thus mediating a 30% enzyme inactivation. Thermophilic bacterium PS3 bears one Fe(III) binding site, which takes up Fe(III) either in the absence or presence of nucleotides and is unable to maintain iron in the redox state of Fe(II) in the absence of ascorbate. Fe(III) bound in thermophilic F1ATPase in a molar ratio 1:1 rapidly reacts with H2O2 mediating a 30% enzyme inactivation. These results support the presence in mitochondrial and thermophilic F1ATPase of a conserved site involved in iron binding and in oxidative inactivation, in which iron exhibits similar redox properties. On the other hand, at variance with thermophilic F1ATPase, the mitochondrial enzyme has the possibility of maintaining one equivalent of Fe(II) in its peculiar ATP-dependent site, besides one equivalent of Fe(III) in the conserved nucleotide-independent site. In this case mitochondrial F1ATPase undergoes a higher inactivation (75%) upon exposure to H2O2. Under all conditions the inactivation is significantly prevented by PBN and DMSO but not by Cu, Zn superoxide dismutase, thus suggesting the formation of OH radicals as mediators of the oxidative damage. No dityrosines, carbonyls or oxidized thiols are formed. In addition, in any cases no protein fragmentation or aggregation is observed upon the treatment with H2O2.

Pictorial essay: thoracic cardiovascular complications of acquired immunodeficiency syndrome.

Patients with acquired immunodeficiency syndrome frequently develop complications of cardiac, pericardial, and thoracic vascular origin. The purpose of this pictorial essay is to review the most common etiologic and diagnostic imaging findings of these diseases. Patients with acquired immunodeficiency syndrome often demonstrate enlargement of the cardiac silhouette on the chest radiograph. While the cause of this finding may be clinically evident, the authors share cases in which chest computed tomography, echocardiography, and nuclear medicine studies better reveal the nature of underlying cardiac and pericardial abnormalities. Thoracic vascular complications, including pulmonary hypertension, pulmonary thromboembolism, and the sequelae of indwelling venous catheters, are also addressed.

Unmasking a patent foramen ovale during recurrent paradoxical cerebral embolism.

A patient with an acute ischemic stroke had an interatrial septal aneurysm shown by transesophageal echocardiography. Interatrial shunting, compatible with a patent foramen ovale, was observed on a follow-up study after a second stroke. This was seen in association with a right atrial thrombus. This case illustrates that an interatrial septal aneurysm serves as a marker for potential interatrial shunting, which can lead to paradoxical cerebral embolism.

Interaction of botulinum and tetanus toxins with the lipid bilayer surface.

The interaction of botulinum neurotoxins serotypes A, B and E (from Clostridium botulinum) and of tetanus neurotoxin (from Clostridium tetani) with the surface of liposomes made of different lipid compositions was studied by photolabelling with a radioiodinated photoactive phosphatidylethanolamine analogue [125I-dipalmitoyl (3,4-azidosalicylamido)phosphatidylethanolamine]. When the vesicles were made of negatively charged lipids (asolectin), each of these neurotoxic proteins was radioiodinated, thus providing evidence for their attachment to the membrane surface. The presence of gangliosides on liposome membranes enhanced fixation of the neurotoxic proteins to the lipid vesicle surface. Both the heavy and light chains of the clostridial neurotoxins were involved in the attachment to the lipid bilayer surface. Each of the toxins tested here attached poorly to liposomes made of zwitterionic lipids (egg phosphatidylcholine), even when polysialogangliosides were present. The data suggest that the binding of botulinum and tetanus neurotoxins to their target neuronal cells involves negatively charged lipids and polysialogangliosides on the cell membrane.

Variation and adaptation of Pseudomonas aeruginosa toxicity to HeLa cells and fibroblasts.

The toxic components of supernatants from Pseudomonas aeruginosa cultures directed against HeLa cells and Staphylococcus aureus were evaluated with the aim of discovering interactions. Supernatants of eight different strains of P. aeruginosa were assayed for cytotoxic activity. All were active against HeLa cells; seven were toxic for S. aureus. On repeated suspension of P. aeruginosa in 0.9% sodium chloride solution, a shift from HeLa cell toxicity to staphylococcal lytic activity occurred along with a change of toxic activity from a high (50,000 +/- 5,000) to a low (8,000 +/- 400) molecular weight (MW) range on gel filtration. Addition of protein to the minimal medium of cultures producing material toxic only for S. aureus reactivated the generation of HeLa cell-toxic material. Cultivation of P. aeruginosa in the presence of HeLa cells and a chloramphenicol supplement produced suppression of the generation of material toxic for S. aureus but facilitated that of HeLa-toxic material of high MW. Adaptation of toxicity against fibroblasts developed only on cocultivation of P. aeruginosa together with S. aureus and in the presence of fibroblasts. Under these conditions a strong lytic activity for S. aureus appeared, even in the presence of chloramphenicol. Chloramphenicol caused the material toxic for fibroblasts to elute at a low MW well separated from that toxic for HeLa cells. In contrast to the high-MW toxic substances, the low-MW material did not induce antibodies after injection into rabbits. This may explain failures of vaccination against P. aeruginosa infection and of serum therapy of homologous sepsis in humans.