Cytomegalovirus (CMV) is one of the most common viral pathogens causing clinical disease in liver transplant recipients, and contributing to substantial morbidity and occasional mortality. CMV causes febrile illness often accompanied by bone marrow suppression, and in some cases, invades tissues including the transplanted liver allograft. In addition, CMV has been significantly associated with an increased predisposition to acute and chronic allograft rejection, accelerated hepatitis C recurrence, and other opportunistic infections, as well as reduced overall patient and allograft survival. To negate the adverse effects of CMV infection on transplant outcome, its prevention, whether through antiviral prophylaxis or preemptive therapy, is an essential component to the management of liver transplant recipients. Two recently updated guidelines have suggested that antiviral prophylaxis or preemptive therapy are similarly effective in preventing CMV disease in modest-risk CMV-seropositive liver transplant recipients, while antiviral prophylaxis is the preferred strategy over preemptive therapy for the prevention of CMV disease in high-risk recipients [CMV-seronegative recipients of liver allografts from CMV-seropositive donors (D+/R-)]. However, antiviral prophylaxis has only delayed the onset of CMV disease in many CMV D+/R- liver transplant recipients, and such occurrence of late-onset CMV disease was significantly associated with increased all-cause and infection-related mortality after liver transplantation. Therefore, a search for better strategies for prevention, such as prolonged duration of antiviral prophylaxis, a hybrid approach (antiviral prophylaxis followed by preemptive therapy), or the use of immunologic measures to guide antiviral prophylaxis has been suggested to prevent late-onset CMV disease. The standard treatment of CMV disease consists of intravenous ganciclovir or oral valganciclovir, and if feasible, reduction in pharmacologic immunosuppression. In one clinical trial, oral valganciclovir was as effective as intravenous ganciclovir for the treatment of mild to moderate CMV disease in solid organ (including liver) transplant recipients. The aim of this article is to provide a state-of-the art review of the epidemiology, diagnosis, prevention, and treatment of CMV infection and disease after liver transplantation.

There was an increase in the Clostridium difficile infection (CDI) rate in our bone marrow transplantation unit. To evaluate the role of unit-based transmission, C. difficile screening was performed on adult patients admitted for hematopoietic stem cell transplantation (HSCT) over a 2-year period, and C. difficile isolates were typed. C. difficile testing was performed using a 2-step C. difficile glutamate dehydrogenase antigen plus toxin A/B enzyme immunoassay (EIA) and cytotoxin assay (or molecular toxin assay). Multilocus sequence typing (MLST) was performed on toxin-positive whole stool samples. A retrospective chart review was performed on all patients with a positive toxin assay. Sixteen of 150 patients (10.7%) had toxigenic C. difficile colonization (CDC) on admission. The overall incidence of CDI within 100 days after HSCT was 24.7% (37 of 150). The median time to diagnosis of CDI was 3.5 days after HSCT. In an adjusted logistic regression model, CDC on admission was a significant risk factor for CDI (odds ratio, 68.5; 95% confidence interval, 11.4 to 416.2). MLST on 22 unit patient toxin-positive stool specimens revealed 15 distinct strain types. Further analysis identified at least 1 potential cross-transmission event; some events may have been missed because of incomplete typing from other specimens. Despite aggressive infection control interventions, there was no decline in the number of CDI cases during the study period. These data suggest that prior CDC plays a major role in CDI rates in this high-risk patient population. It remains unclear if CDI was cross-transmitted in the unit.

Co-trimoxazole (CTX) causes various forms of severe cutaneous adverse reactions (SCARs). This case-control study was conducted to investigate the involvement between genetic variants of human leukocyte antigen (HLA) and CYP2C9 in CTX-induced SCARs, including Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and drug reaction with eosinophilia and systemic symptoms (DRESS) in Thai patients. Thirty cases of CTX-induced SCARs were enrolled and compared with 91 CTX-tolerant controls and 150 people from the general Thai population. Cases comprised 18 SJS/TEN and 12 DRESS patients. This study demonstrated that genetic association of CTX-induced SCARs was phenotype-specific. HLA-B*15:02 and HLA-C*08:01 alleles were significantly associated with CTXinduced SJS/TEN, whereas the HLA-B*13:01 allele was significantly associated with CTX-induced DRESS. In addition, a significant higher frequency of HLA-A*11:01-B*15:02 and HLA-B*13:01-C*03:04 haplotypes were detected in the group of CTX-induced Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and DRESS cases, respectively. Genetic association of CTX-induced SCARs is phenotype-specific. Interestingly, these association was observed only in HIV-infected patients but not in non-HIV-infected patients.

bRothia mucilaginosa is increasingly recognized as an emerging opportunistic pathogen associated with prosthetic device infections. Infective endocarditis is one of the most common clinical presentations. We report a case of R. mucilaginosa prosthetic valve endocarditis and review the literature of prosthetic device infections caused by this organism. CASE REPORTA 36-year-old man was admitted to the hospital in January 2012 with a chief complaint of left foot pain for 1 week. He described redness and swelling on the dorsum of his left foot. He denied trauma to the foot. He had been taking acetaminophen for pain intermittently without relief. He denied fever or chills, visual changes, back pain, muscle weakness, or numbness. He had a history of Streptococcus mitis mitral valve endocarditis and required mechanical mitral valve replacement in 2009. He had no history of peripheral vascular disease or claudication. He had no known drug allergies. His home medications included warfarin, methadone, and acetaminophen. He was an active intravenous heroin user. He was a former tobacco user with a 5-pack-year history who had quit 7 years before.On examination, the patient appeared well. His temperature was 100.9°F (38.3°C), pulse 108 beats per minute, blood pressure 133/64 mm Hg, and respirations 20 per minute. Cardiovascular examination revealed normal S1 and S2 and no murmurs, rubs, or gallops. The dorsum of the left foot had mild erythema, slight edema, and point tenderness of the mid-dorsal region. The left dorsalis pedis pulse was easily palpable. Skin examination revealed track marks at the right antecubital fossa. The remainder of the examination was normal. Laboratory studies revealed a white blood cell count of 20 ϫ 10 3 cells/mm 3 (reference range, 4 ϫ 10 3 to 11 ϫ 10 3 /mm 3 ), neutrophils at 88%, creatinine at 0.8 mg/dl, and an erythrocyte sedimentation rate of 35 mm/h (reference range, 0 to 10 mm/h). Other routine laboratory tests were normal. A leftfoot radiograph revealed no fracture, and an ultrasound of the left lower extremity revealed no deep vein thrombosis. Intravenous vancomycin and piperacillin-tazobactam were administered empirically for a presumptive diagnosis of left-foot cellulitis. The fever resolved, but the patient had persistent pain in the left foot, which subsequently turned blue and felt cold. Computed tomographic angiography revealed left popliteal artery thrombosis. A left popliteal thromboembolectomy was performed on day 4 of hospitalization. The pathology of the left popliteal thrombus revealed an organized thrombus with clusters of Gram-positive cocci. On day 4 of hospitalization, two sets of blood cultures obtained on the day of admission grew Rothia mucilaginosa from the aerobic bottles only.The organism was identified based upon biochemical tests, automated identification platforms (Phoenix system), and phenotypic characteristics. Gram stain revealed Gram-positive cocci that were catalase negative and grew sticky "staph-like" colonies which were whitish to gray in color, nonhemolyt...