br Authors Contributions br Acknowledgements We thank the
Acknowledgements We thank the EpiGen Operational Management Group for their project management and Dr. Irma Silva Zolezzi, Nestlé Research Center, for helpful discussion of the manuscript. We also thank all the families that took part in The Raine study and the Raine Study team, which includes data collectors, cohort managers, clerical staff, research scientists, and volunteers. This work was supported by the Raine Medical Research Foundation; Healthway, Western Australia; The Telethon Kids Institute, University of Western Australia (UWA); Faculty of Medicine, Dentistry and Health Sciences, University of Western Australia (UWA); Women and Infants Research Foundation (UWA); Curtin University; and The Australian National Health and Medical Research Council (NHMRC). RCH is supported by a NHMRC Fellowship.
Introduction Mycoplasma hominis (M. hominis) is a mollicute that colonizes the urogenital tract and occasionally causes invasive disease. Extra-genital infections with this organism occur primarily in immunosuppressed persons. M. hominis has been linked to pregnancy-related complications and causes meningitis and pneumonia in neonates (Cassell et al., 1991; Samra et al., 2002; Waites et al., 1988). M. hominis is not visualizable by gram stain due to its lack of a cell wall, and although it may grow on standard aerobic or tegaserod cost bacterial culture plates, this method is insensitive and requires highly experienced laboratory personnel to recognize colonies of M. hominis. M. hominis-specific culture may be performed, but are not widely available, and even if they are available, is not rapid. The route of acquisition of M. hominis in patients who undergo cardiothoracic transplantation has not been defined. In two prior reports in Chest the authors speculated 1) the organism entered the bloodstream (though blood cultures were negative) of a lung transplant recipient who developed pleural and pulmonary infection with M. hominis. These authors speculated manipulation of the urinary tract with a Foley catheter elicited invasion of lung tissue damaged by transplantation (Lyon et al., 1997) and 2) an 18 year old women developed diffuse alveolar hemorrhage following bone marrow transplant due to unproven airway or urinary tract colonization (Kane et al., 1994). Herein, we describe seven new cases of M. hominis infection in cardiothoracic transplant recipients and review the literature on the topic. We highlight the unique clinical presentation of M. hominis in this patient population and present evidence suggesting that this infection may be donor-transmitted. M. hominis should be considered in the etiological diagnosis of surgical site infections, mediastinitis and pleuritis after lung or heart-lung transplantation; use of M. hominis-specific PCR may expedite diagnosis.
Discussion M. hominis infection in cardiothoracic transplant recipients has been uncommonly reported. The true infection rate may be underestimated in view of difficulties in detecting the organism in clinical specimens and in the use of antibiotic prophylaxis and empiric antimicrobial regimens, such as fluoroquinolones, that do target M. hominis. Cardiothoracic transplant patients sustain all of the risks for infection generally encountered in the routine practice of cardiovascular surgery, including Staphylococcus species, Pseudomonas, and Serratia, but fungi especially Aspergillus species and Candida contribute importantly (Stinson and Oyer, 1995). Donor transmission of infection remains important. Surveillance cultures of donor and recipient, and antimicrobial prophylaxis remain the cornerstone of infection prevention. In the report herein, we note infection with M. hominis in the absence of other known infection. The manifestations were often delayed after transplantation by several weeks, and included pleuritis with cellulitis, trapped lung, delayed airway anastomotic healing, and aortic and sternal dehiscence. Treatment included surgical intervention and long-term antibiotics.