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Biomedical subjects

J E Mangino

Publications and source records attributed to J E Mangino.

10 recordsLinked to original sources
PubMed2000

A prosthetic breast implant infected with Mycobacterium fortuitum.

Augmentation mammaplasty is a common operation performed in the United States. Postoperative wound infections are rare, but can be devastating. Most often, bacteria from the normal skin flora cause these infections, but more atypical organisms can lead to similar situations. The authors present a case of a prosthetic breast implant infected with Mycobacterium fortuitum after augmentation mammaplasty. The patient, diagnosis, and treatment are discussed so that others may recognize and treat this entity successfully before encountering major complications. Although it is an infrequent occurrence, plastic surgeons, infectious disease specialists, and primary care doctors who may see postoperative wound infections should be aware of this potential pathogen. It is important in any postimplant infection and especially crucial in cases of unresolving or recurrent infections with unusual or even clear drainage. With proper identification through acid-fast smear and culture, multiagent therapy can be initiated early. Additional complications, including implant removal, may thus be avoided.

Adult↗
PubMed1997

Genotypic investigation of multidrug-resistant Acinetobacter baumannii infections in a medical intensive care unit.

Multi-resistant Acinetobacter baumannii isolates obtained from 13 hospitalized patients over a six-month period were evaluated. One patient had an isolate susceptible only to imipenem; the next three had isolates susceptible to imipenem and ampicillin/sulbactam; the next six patients had isolates which were susceptible to imipenem, amikacin, and ampicillin/sulbactam; while the final three patients had isolates which were susceptible to imipenem and ampicillin/sulbactam. Ten patients died, five within 10 days of a positive culture. Five of six patients with bacteraemia succumbed to the infection. DNA extracted from all isolates was amplified by polymerase chain reaction using four random primers (RAPD). The resulting band patterns were compared and strains identified. In addition, all isolates were biotyped. RAPD analysis and biotyping showed that there were two distinct strains involved. The first four patients were infected with one strain (genotype ¿A', biotype 9), the subsequent nine patients were infected with a second strain (genotype ¿B', biotype 1). These results suggested that there was patient-to-patient spread of strains. Institution of, and strict adherence to, isolation procedure and other infection control practices controlled the spread of infection. These data emphasize the need for active surveillance for multidrug-resistant organisms in critically ill patients, and the value of molecular typing of strains in a hospital setting to investigate spread of infection.

Acinetobacter↗
PubMed1997

Effects of the 5-lipoxygenase inhibitor A-64077 on intestinal hypothermic organ preservation injury.

The effects of the orally active selective 5-lipoxygenase inhibitor Zileuton (A-64077, (N-1(1-benzo{b}thien-2-ylethyl)-N-hydroxyurea) were studied in a canine model of hypothermic intestinal organ ischemia-reperfusion (I/R) injury (transplant preservation injury). Forty-eighty hours of hypothermic intestinal ischemia utilizing Collin's flush, followed by 1 hr of reperfusion (transplantation) in A-64077-treated animals, resulted in a 3-fold increase in intestinal oxygen uptake and blood flow relative to the untreated controls. The postreperfusion movement of fluid from the microcirculation into the intestinal lumen significantly increased in the control animals at reperfusion, and A-64077 treatment dramatically exacerbated this phenomenon. Mucosal neutrophil infiltration, or the processes leading to infiltration, significantly increased after 48 hr of cold ischemia and 1 hr of normothermic reperfusion in the untreated animals. A similar response was observed in A-64077-treated dogs, but the absolute levels of MPO were 10-fold less relative to untreated animals, including intestinal tissue obtained before I/R. Hypothermic I/R injury in this model resulted in severe histologic injury. A-64077-treated dogs, however, demonstrated significant improvements in histologic injury. Mucosal synthesis of LTB4 rose significantly after cold I/R injury and was abrogated by A-64077 treatment. The synthesis of PGE2 significantly increased after cold I/R in both untreated and A-64077-treated dogs. The increase in PGE2 production after hypothermic I/R in the A-64077-treated animals was higher relative to the untreated control animals. In conclusion, this study indicates that arachidonic acid metabolism via the 5-lipoxygenase pathway plays a significant role in the pathophysiology of hypothermic intestinal I/R injury. Furthermore, the 5-lipoxygenase inhibitor A-64077 possesses favorable pharmacologic and biologic responses in this intestinal injury and should be considered in the clinical amelioration of intestinal transplantation preservation injury.

Animals↗
PubMed1996

Characterization of hypothermic intestinal ischemia-reperfusion injury in dogs. Effects of glycine.

The effects of 48 hr of hypothermic (4 degrees C ischemia) and short-term reperfusion. (I-R) on intestinal function and metabolism were studied in dogs utilizing Collins flush alone or with the putative cytoprotectant amino acid, glycine. Intestinal blood flow after hypothermic ischemia in Collins-flushed segments briefly rose at reperfusion, rapidly declined after 5 min, and plateaued over the 60-minute reperfusion period. Paired intestinal segments flushed with 5 mM glycine demonstrated parallel changes in blood flow over the reperfusion period, but the blood flow values were significantly higher (100-300%), relative to the Collins segments. Intestinal oxygen consumption (VO2) was about 50% of normal nonischemic intestinal segments at all times after reperfusion. The glycine-flushed intestinal segments significantly consumed about 100% more oxygen, relative to the paired control intestines. Intestinal fluid and protein flux into the lumen significantly increased after I-R in both glycine- and Collins-flushed segments. Mucosal tissue myeloperoxidase (MPO) activity, a biochemical marker of neutrophils, significantly increased after 48 hr of cold ischemia with Collins flush and 1 hr of reperfusion, relative to tissue obtained before ischemia. The reperfusion-induced increase in MPO activity was abolished in intestinal segments flushed with glycine. Mucosal synthesis of the chemoattractant leukotriene B4 (LTB4) significantly increased after I-R and glycine flush abolished these increases. Nitric oxide synthesis by mucosal tissue in Collins-flushed segments subjected to 48 hr of hypothermic ischemia and 1 hr of reperfusion was significantly higher, compared with nonischemic tissue or mucosal tissue subjected to cold ischemia without reperfusion. Glycine flush did not alter this pattern of NO synthesis. Light microscopic analysis in both Collins- and glycine-flushed segments revealed that intestinal hypothermic ischemia and reperfusion caused significant morphologic changes characterized by loss of villus epithelium, decreased villus height, and venous congestion. These data indicate that glycine significantly improve oxygenation after hypothermic ischemia and reperfusion and prevented the I-R-induced increase in tissue neutrophil infiltration and leukotriene synthesis.

Animals↗
PubMed1996

Arachidonic acid metabolism in intestinal hypothermic preservation injury.

The effect of hypothermic intestinal ischemia and short-term reperfusion on mucosal arachidonic acid metabolism was studied in a dog model of intestinal preservation injury. Canine intestinal segments were flushed with cold Collins solution, cold stored (4 degrees C) for either 24 or 48 h, and subsequently reperfused in the donor for 1 h. Samples of intestinal mucosa obtained before ischemia, after the ischemia period, and after the reperfusion period were placed into tissue culture, and arachidonic acid metabolites were measured in the tissue incubation media. Prostaglandin E2 (PGE2) and prostacyclin (PGI2) production significantly increased after 24 h of cold ischemia and after 1 h of reperfusion, respectively. Intestines cold stored for 48 h and after 1 h of reperfusion produced significantly elevated quantities of thromboxane B2, PGI2, PGE2, and leukotriene B4, relative to the production rates from nonischemic control tissue or tissue subjected to 48 h of hypothermic ischemia without reperfusion. Mucosal production of thiol ether leukotrienes (LTC4, LTD4, LTE4) was not altered by ischemia or reperfusion at any time of cold ischemia. The synthesis of the lipoxygenase product 12-hydroxyeicosatetraenoic acid (12-HETE) was not altered by hypothermic ischemia or reperfusion, but this arachidonate metabolite was produced by small intestinal mucosa in the greatest quantities. Specifically, nanogram quantities of 12-HETE were produced by intestinal mucosa compared to picogram quantities of the other metabolites measured. Significant synthesis of the delta lactone derivative of 5-hydroxyeicosatetraenoic acid was detected by HPLC in many tissue samples undergoing 48 h of ischemia and reperfusion, relative to nonischemic tissue samples. In conclusion, significant increases in arachidonate cyclooxygenase and lipoxygenase metabolites have been identified in intestinal mucosa subjected to long-term hypothermic ischemia and short-term reperfusion. Synthesis of these products increases with the duration of cold ischemia and may play a role in intestinal preservation injury.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗