Infected pulmonary aneurysm following pulmonary artery banding

2016 ◽  
Vol 25 (9) ◽  
pp. 642-644
Author(s):  
Yuki Nakayama ◽  
Yusuke Iwata ◽  
Toshihide Nishimori ◽  
Takamasa Takeuchi

A 1-month-old girl, diagnosed with a common atrioventricular canal, moderate atrioventricular valvular regurgitation, and pulmonary hypertension, underwent pulmonary artery banding. Postoperatively, methicillin-resistant Staphylococcus aureus wound infection was treated with antibiotics. One month later, emergency surgery was performed for oozing rupture of an infected pulmonary aneurysm. The pulmonary aneurysm was completely resected, the banding tape was removed, and pulmonary angioplasty was performed to create pulmonary stenosis without using foreign material. Methicillin-resistant Staphylococcus aureus was cultured from the resected tissues and banding tape. The patient was discharged after antibiotic administration. Correction was performed at 1 year of age, and she remains well.

2011 ◽  
Vol 135 (8) ◽  
pp. 1057-1060
Author(s):  
Jared A Hershenson ◽  
Peter B Baker ◽  
Daniel G Rowland

Myocardial abscess perforation is an extremely rare complication of infective endocarditis. We present a case of a 12-month-old infant who developed community-associated methicillin-resistant Staphylococcus aureus bacteremia after an incision and drainage of a skin abscess. He subsequently developed septic emboli to the brain and lungs, and a myocardial cavity in the outlet portion of the interventricular septum. The cavity ruptured 4 days after diagnosis and created a left ventricle to pulmonary artery fistulous communication. The patient died secondary to embolic complications to the brain. We are not aware of any other cases of myocardial abscess rupture in this location of the heart, in a patient of this age, or due to infection with community-associated methicillin-resistant S aureus.


2020 ◽  
Vol 9 (2) ◽  
pp. 49-59
Author(s):  
Kristin Yu ◽  
Lee Song ◽  
Hyunwoo Paco Kang ◽  
Hyuk-Kwon Kwon ◽  
Jungho Back ◽  
...  

Aims To characterize the intracellular penetration of osteoblasts and osteoclasts by methicillin-resistant Staphylococcus aureus (MRSA) and the antibiotic and detergent susceptibility of MRSA in bone. Methods Time-lapse confocal microscopy was used to analyze the interaction of MRSA strain USA300 with primary murine osteoblasts and osteoclasts. The effects of early and delayed antibiotic treatments on intracellular and extracellular bacterial colony formation and cell death were quantified. We tested the effects of cefazolin, gentamicin, vancomycin, tetracycline, rifampicin, and ampicillin, as well as agents used in surgical preparation and irrigation. Results MRSA infiltrated bone-resident cells within 15 to 30 minutes. Penetration was most effectively prevented with early (i.e. 30 minutes) antibiotic administration. The combined administration of rifampicin with other antibiotics potentiated their protective effects against MRSA-induced cytotoxicity and most significantly reduced extracellular bacterial bioburden. Gentamicin-containing compounds were most effective in reducing intracellular MRSA bioburden. Of the surgical preparation agents evaluated, betadine reduced in vitro MRSA growth to the greatest extent. Conclusion The standard of care for open fractures involves debridement and antibiotics within the first six hours of injury but does not account for the window in which bacteria penetrate cells. Antibiotics must be administered as early as possible after injury or prior to incision to prevent intracellular infestation. Rifampicin can potentiate the capacity of antibiotic regimens to reduce MRSA-induced cytotoxicity. Cite this article: Bone Joint Res. 2020;9(2):49–59.


2013 ◽  
Vol 109 (04) ◽  
pp. 684-695 ◽  
Author(s):  
Adriana Vieira de Abreu ◽  
Jeffrey T. Holloway ◽  
James E. Marvin ◽  
Bjoern F. Kraemer ◽  
Guy A. Zimmerman ◽  
...  

SummaryMethicillin-resistant Staphylococcus aureus (MRSA) induces a prothrombotic and pro-inflammatory milieu. Although timely antibiotic administration in MRSA sepsis may improve outcomes by arresting bacterial growth, the effects of antibiotics on mitigating injurious thrombo-inflammatory cellular responses remains unexplored. Using a newly developed human whole blood model and an in vivo mouse model of MRSA infection, we examined how antibiotics inhibit MRSA induced thrombo-inflammatory pathways. Human whole blood was inoculated with MRSA. Thrombin generation and inflammatory cytokine synthesis was measured in the presence or absence of linezolid and vancomycin. C57BL/6 mice were injected with MRSA and the effect of vancomycin administration was examined. MRSA accelerated thrombin generation in a time- and concentration-dependent manner and induced the release of cytokines, including interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1. The increase in thrombin generation and inflammatory responses was mediated through the synthesis of tissue factor and cytokines, respectively, and the release of microparticles. The early administration of antibiotics restored normal thrombin generation patterns and significantly reduced the synthesis of cytokines. In contrast, when antibiotic administration was delayed, thrombin generation and cytokine synthesis were not significantly reduced. In mice infected with MRSA, early antibiotic administration reduced thrombin anti-thrombin complexes and cytokine synthesis, whereas delayed antibiotic administration did not. These data provide novel mechanistic evidence of the importance of prompt antibiotic administration in infectious syndromes.


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