Background: Solid-organ transplantation (SOT) has become the preferred approach to treat end-stage organ disease. While preventive strategies have reduced the risk for classical opportunistic infections, bacterial -particularly bloodstream infections (BSI)- remain the most frequent short-term complications in SOT recipients and potentially life threatening. Our objective was to analyze the epidemiology, microbiological characteristics and risk factors associated with morbidity and mortality of BSI in SOT during the first 90 days after transplantation. Methods & Materials: Prospective, observational, multicenter study. Through a single data collection record, all BSI in SOT during the first 90 days post-transplantation were enrolled between May 2016 and September 2017. Results: We documented 104 episodes of BSI in: kidney (67%), liver (13%), heart (8%) and other (12%) transplant recipients. Thymoglobulin plus corticoids was the most common induction immunosuppression (43%) in kidney transplant, while tacrolimus, steroids and micofenolic acid was for maintenance (68.5%). 34% of the patients were colonized by multi-drug resistant organisms (MDRO) 12 months prior to BSI, 29% had a previous infection by these MDRO, and 71% received antibiotics 90 days prior to transplantation. Of the 104 BSIs, 92.3% were of nosocomial acquisition and 20 patients (19.2%) had more than one BSI. Secondary bacteremias accounted for 85% of the episodes, being urinary (56.7%) and surgical site infection (12.5%) the most frequent foci. Gram-negative bacilli (GNB) caused 83% of the BSI, with Klebsiella pneumoniae registered as the most common agent (33%). 60% of the specimens were MDRO, being extended spectrum b-lactamase (ESBL) the most frequent mechanisms (59.7%), followed by carbapenemase production (15%). There was no significant difference in clinical symptoms, signs and severity (measured by Pitt and APACHE II scores) between patients infected by MDRO and non-MDRO. An adequate empiric antibiotic therapy was registered in 80% of non-MDRO BSI, and 73% in MDRO BSI (p = 0.67) There was no difference in 30-day overall mortality between both groups (24% vs 21%, p = 0.68) Conclusion: It is essential to know the epidemiology of BSI and the mechanisms of resistance of the MOs in order to improve prophylaxis and empirical therapies, to finally reduce the impact of these infections in mortality.

Background: In recent years, a significant increase in invasive infections by multi-drug resistant bacteria (MDR) in oncohaematological (OH) patients has been documented in our country, mainly those caused by gram-negative bacilli, such as KPC. Research has proved connection between colonization and bacteraemia by MDR. Active surveillance of colonization might help identify patients at risk. Objective: analyse the relation between MDR colonization and bacteraemia by the same MDR previously detected in a swab test. Methods & Materials: Active surveillance data of MDR colonization and bacteraemic infections (MRSA, VRE, Carbapenemase producing Klebsiella pneumoniae (KPC), Acinetobacter baumanii, Pseudomonas aeruginosa) was collected prospectively from OH hospitalised patients from April 2016 to September 2017. Nasal, rectal, axillary and inguinal swabs were carried out on admission and once weekly until discharge. The results of the categorical variables are shown as percentages, and the ones of numeric variables as mean and standard deviation. In order to compare proportions, the chi-square test was used. Relative risk (RR) was calculated as well as confidence intervals (CI) for 95%. A p < 0.05 has been considered significant. Results: 913 surveillance swabs were carried out in 212 patients. 55% men, average age: 53.2 years old. Underlying diseases: NHL 30%, MM 22%, AML 18%, ALL 12%, MDS 5%, HL 4%, others 9%. Initial swabs were positive in 17/212 (8%) patients. Follow-up monitoring swabs were made in 137 patients, out of which 37/137 (25%) were positive. We documented 17 bacteraemias/51 colonized patients (33%), 8/17 bacteraemias (47%) caused by MDR, and 56 bacteraemias/161 non-colonized patients (34.7%), 10/56 (17%) caused by MDR (p 0.03). The association between colonization by MDR and MDR bacteraemia was significant: p 0.02; OR: 4.08; IC 95%: 1.2 – 13.21; PPV: 47%; NPV: 82%; S: 44% y E: 83%. Only in the subgroup of patients colonized by KPC there was a significant association with bacteraemia caused by the same bacteria: p 0,0001; RR: 6; IC 95%: 2.9- 12.1; PPV: 85%; NPV: 85%; S: 42% y E: 97%. Conclusion: In our OH-patient population, we found association between colonization and bacteraemia by KPC. Surveillance of MDR colonization, particularly KPC, would allow to select the best empirical treatment, and reduce associated mortality.

Cytomegalovirus is the most important viral infection in kidney transplants, but rarely affects the allograft after the sixth month posttransplantation. We present a patient who developed renal failure eighteen months posttransplant; a kidney biopsy showed cytomegalovirus inclusions, acute tubular necrosis and mild interstitial nephritis. After intravenous ganciclovir, renal function transiently improved. Cytomegalovirus pp65 antigen was weekly reported as negative. One month later another biopsy was performed due to renal failure. The findings were consistent with tubular atrophy and severe interstitial nephritis. No cytomegalovirus cellular inclusions were found on histology, including immunohistochemical and polymerase chain reaction studies; pp65 antigen studies were persistently negative. Despite an attempt to recover renal function with steroid therapy, the patient restarted hemodialysis 20 months posttransplantation. This report suggests that cytomegalovirus should be considered as a late cause of kidney failure even in the absence of infection-related symptoms. The irreversible allograft damage can be caused despite the successful eradication of the virus with intravenous ganciclovir.

Thirty patients with endocarditis caused by penicillin-susceptible streptococci were enrolled in one of two groups in this study. Fifteen patients received ceftriaxone (2 g once daily) for 4 weeks; the other 15 received the same dosage of ceftriaxone for 2 weeks and then received oral amoxicillin (1 g four times a day) for 2 weeks. For the 27 patients treated predominantly as out-patients, 380 days of hospitalization were avoided. Clinical cure was achieved for all patients in both groups. We conclude that ceftriaxone, alone or followed by a course of amoxicillin, is an efficacious mode of treatment for infective endocarditis caused by penicillin-susceptible streptococci. Treatment with these agents can be administered predominantly on an outpatient basis.