Case Report: Successful Treatment of Recurrent Urinary Tract Infection Due to Extensively Drug-Resistant Klebsiella Pneumoniae in a Kidney Transplant Recipient Using Chloramphenicol.

Effective therapies for multidrug-resistant (MDR) microorganisms, especially Gram-negative bacteria, are becoming rare. Also, solid-organ transplant recipients are at high risk of MDR Gram-negative bacilli infection. Urinary tract infections are the most frequent bacterial infections in kidney transplant recipients and are an important cause of mortality after renal transplantation. We describe a case of complicated urinary tract infection in a kidney transplant patient due to extensively drug-resistant (XDR) K. pneumoniae treated successfully with a regimen comprising a combination of chloramphenicol and ertapenem. We do not recommend chloramphenicol as a first-line choice for treating complicated urinary tract infections. Still, we believe it is an alternative for infections caused by MDR and/or XDR pathogens in renal transplant patients, as other options are nephrotoxic.

Genetic description of VanD phenotype vanA genotype in vancomycin-resistant Enterococcus faecium isolates from a Bone Marrow Transplantation Unit.

BACKGROUND: Vancomycin-resistant Enterococcus faecium (VREfm) is an important agent of hospital-acquired infection. VanA phenotype is characterized by resistance to high levels of vancomycin and teicoplanin and is encoded by the vanA gene, whereas VanD phenotype is characterized by resistance to vancomycin and susceptibility or intermediate resistance to teicoplanin; however, some isolates carry a VanD phenotype with a vanA genotype, but there are many gaps in the knowledge about the genetic mechanisms behind this pattern. OBJECTIVE: To characterize the genetic structure, clonality, and mobile genetic elements of VRE isolates that display a VanD-vanA phenotype. RESULTS: All vanA VRE-fm isolates displayed minimum inhibitory concentration (MIC) for vancomycin > 32µg/mL and intermediate or susceptible MIC range for teicoplanin (8-16µg/mL). The isolates were not clonal, and whole-genome sequencing analysis showed that they belonged to five different STs (ST478, ST412, ST792, ST896, and ST1393). The absence of some van complex genes were observed in three isolates: Ef5 lacked vanY and vanZ, Ef2 lacked vanY, and Ef9 lacked orf1 and orf2; moreover, another three isolates had inverted positions of orf1, orf2, vanR, and vanS genes. IS1542 was observed in all isolates, whereas IS1216 in only five. Moreover, presence of other hypothetical protein-encoding genes located downstream the vanZ gene were observed in six isolates. CONCLUSION: VRE isolates can display some phenotypes associated to vanA genotype, including VanA and VanB, as well as VanD; however, further studies are needed to understand the exact role of genetic variability, rearrangement of the transposon Tn1546, and presence of insertion elements in isolates with this profile.

Staging liver fibrosis after severe yellow fever with ultrasound elastography in Brazil: A six-month follow-up study.

BACKGROUND: Yellow fever (YF) is a hemorrhagic disease caused by an arbovirus endemic in South America, with recent outbreaks in the last years. Severe cases exhibit fulminant hepatitis, but there are no studies regarding its late-term effects on liver parenchyma. Thus, the aim of this study was to determine the frequency and grade of liver fibrosis in patients who recovered from severe YF and to point out potential predictors of this outcome. METHODOLOGY/PRINCIPAL FINDINGS: We followed-up 18 patients who survived severe YF during a recent outbreak (January-April 2018) in Brazil using ultrasound (US) with shear-wave elastography (SWE) at 6 months after symptoms onset. No patient had previous history of liver disease. Median liver stiffness (LS) was 5.3 (4.6-6.4) kPa. 2 (11.1%) patients were classified as Metavir F2, 1 (8.3%) as F3 and 1 (8.3%) as F4; these two last patients had features of cardiogenic liver congestion on Doppler analysis. Age and cardiac failure were associated with increased LS (p = 0.036 and p = 0.024, respectively). SAPS-3 at ICU admission showed a tendency of association with significant fibrosis (≥ F2; p = 0.053). 7 patients used sofosbuvir in a research protocol, of which none showed liver fibrosis (p = 0.119). CONCLUSIONS/SIGNIFICANCE: We found a low frequency of liver fibrosis in severe YF survivors. US with SWE may have a role in the follow up of patients of age and / or with comorbidities after hospital discharge in severe YF, a rare but reemergent disease.

Impact of human immunodeficiency virus infection on mortality of patients who acquired healthcare associated-infection in critical care unit.

To evaluate 30-day mortality in human immunodeficiency virus (HIV) and non-HIV patients who acquired a healthcare-associated infection (HAI) while in an intensive care unit (ICU), and to describe the epidemiological and microbiological features of HAI in a population with HIV.This was a retrospective cohort study that evaluated patients who acquired HAI during their stay in an Infectious Diseases ICU from July 2013 to December 2017 at a teaching hospital in Brazil.Data were obtained from hospital infection control committee reports and medical records. Statistical analysis was performed using SPSS and a multivariate model was used to evaluate risk factors associated with 30-day mortality. Epidemiological, clinical, and microbiological characteristics of HAI in HIV and non-HIV patients and 30-day mortality were also evaluated.Among 1045 patients, 77 (25 HIV, 52 non-HIV) patients acquired 106 HAI (31 HIV, 75 non-HIV patients). HIV patients were younger (45 vs 58 years, P = .002) and had more respiratory distress than non-HIV patients (60.0% vs 34.6%, P = .035). A high 30-day mortality was observed and there was no difference between groups (HIV, 52.0% vs non-HIV, 54.9%; P = .812). Ventilator-associated pneumonia (VAP) was more frequent in the HIV group compared with the non-HIV group (45.2% vs 26.7%, P = .063), with a predominance of Gram-negative organisms. Gram-positive agents were the most frequent cause of catheter associated-bloodstream infections in HIV patients. Although there was a high frequency of HAI caused by multidrug-resistant organisms (MDRO), no difference was observed between the groups (HIV, 77.8% vs non-HIV, 64.3%; P = .214). Age was the only independent factor associated with 30-day mortality (odds ratio [OR]: 1.05, 95% confidence interval [CI]: 1.01-1.1, P = .017), while diabetes mellitus (OR: 3.64, 95% CI: 0.84-15.8, P = .085) and the Sequential Organ-Failure Assessment (SOFA) score (OR: 1.16, 95% CI: 0.99-1.37, P = .071) had a tendency to be associated with death.HIV infection was not associated with a higher 30-day mortality in critical care patients with a HAI. Age was the only independent risk factor associated with death. VAP was more frequent in HIV patients, probably because of the higher frequency of respiratory conditions at admission, with a predominance of Gram-negative organisms.

Colistin-resistant Enterobacteriaceae infections: clinical and molecular characterization and analysis of in vitro synergy.

We described 27 polyclonal colistin-resistant Enterobacteriaceae (MIC 4-16 µg/mL) infections (12 pneumonia, 12 urinary tract infection (UTI), two Bacteremia, and one skin/soft tissue infection) in which 74% harbored KPC. The isolates were polyclonal, 6 STs were identified and the colistin resistance was due to chromosome mutations. Eight patients with UTI received monotherapy, and combination therapy was given to 19 patients. Overall mortality was 37%. In vitro synergy using time-kill assay was observed in 14 of 19 (74%) isolates tested; the synergistic effect was observed for almost all isolates for the combination of three drugs: colistin, amikacin, and tigecycline. The Kaplan-Meier survival curve showed no significant difference comparing combination therapy with 2, 3, or more drugs and risk factors associated with death were dialysis and shock. These findings reinforce the fact that colistin in combination with other classes of drugs can be useful in treating infections caused by colistin-resistant CRE.