Background Periprosthetic joint infection (PJI) is a severe complication from the patient's perspective and an expensive one in a value-driven healthcare model. Risk stratification can help identify those patients who may have risk factors for complications that can be mitigated in advance of elective surgery. Although numerous surgical risk calculators have been created, their accuracy in predicting outcomes, specifically PJI, has not been tested.
Campath-1H induction for renal transplantation appears to have a low incidence of associated infectious complications when compared to historical regimens.
Sera of young children who had had a primary infection with influenza A virus or were immunized with a live attenuated influenza A virus vaccine were examined for antibody responses that neutralized virus or enhanced uptake of virus into Fc receptor-bearing cells, because antibodies that enhance uptake of influenza virus into Fc receptor-bearing cells have been reported using mouse immune serum and monoclonal antibodies. The neutralizing antibody titers to the homologous infecting virus and to another H1N1 virus isolated several years later were higher after natural infection than after infection with the live attenuated virus. Natural infection and the attenuated vaccine induced antibodies that enhanced uptake of homologous virus and H1N1 virus isolated several years later. These results demonstrate that primary influenza A virus infection results in the induction of infection-enhancing antibodies.
Culture-negative bacterial endocarditis may be attributed to fastidious microorganisms, prior institution of antibiotic treatment, or both. We describe a case of culture-negative endocarditis in which a modified Steiner stain revealed bacterial structures in the resected heart valve material. Prompted by this finding, broad-range polymerase chain reaction (PCR) amplification of small-subunit ribosomal DNA (16S rDNA) was performed, and Cardiobacterium hominis sequences were detected. This case demonstrates the usefulness of both the Steiner stain and broad-range direct molecular amplification as supplemental diagnostic tools in identification of otherwise unexplained infections.
Nocardia spp. are common environmental organisms that, to our knowledge, have never been implicated as causing an implantable defibrillator or pacemaker infection. We describe a 70-year-old male with a recent implantable cardiac defibrillator revision and subsequent device infection and bacteremia caused by a Nocardia nova complex isolate.
CASE REPORTA 70-year-old-male with long-standing diabetes, ischemic cardiomyopathy, and inducible ventricular tachycardia presented with inappropriate shocks due to fracture of his implantable cardiac defibrillator (ICD) lead 3 years postimplantation. He underwent a procedure in which his fractured lead was abandoned and a new lead and pulse generator were implanted.He tolerated the replacement procedure well and approximately 2 weeks later noticed swelling around the site. He presented to a surgeon, who noted swelling around the site and aspirated serosanguinous fluid from the pocket. A routine aerobic culture of this fluid was negative. The swelling continued, and 1 week later the patient returned to the surgeon, who again aspirated the site. He returned for a third visit 1 week later with additional symptoms, including swelling, erythema, tenderness, fevers, and chills. The pocket was again aspirated, and the patient was transferred to our institution for further evaluation.Upon arrival at Geisinger Medical Center, the patient had a temperature of 38.4°C, heart rate of 79/min, respirations of 16/min, and an admission blood pressure of 114/70. Two routine peripheral blood cultures were collected, and vancomycin was initiated for suspected defibrillator pocket infection. Aerobic cultures from the second and third aspiration as well as from the admission blood cultures grew a pure culture of a beaded, branching gram-positive bacillus identified as a Nocardia nova complex isolate. Vancomycin was discontinued, and treatment was begun with trimethoprim-sulfamethoxazole at a dose of 8 mg/kg of body weight/day of trimethoprim divided twice daily. A transesophageal echocardiograph showed no evidence of endocarditis. The newly implanted ICD system and previously abandoned lead were removed to optimally treat the patient's infection. The pocket had 10 ml of purulent bloody fluid as well as necrotic tissue removed during reimplantation. The patient completed 6 weeks of oral antibiotic treatment and had his defibrillator replaced approximately 2 months later. There has been no recurrence to date.
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