Emergence of OXA-48-type carbapenemase-producing Enterobacteriaceae in German hospitals.

Nine carbapenem-resistant Enterobacteriaceae isolates collected from eight patients in five German hospitals were investigated. Six isolates produced the OXA-48 carbapenemase, and three isolates produced OXA-162, which is a point mutant form of OXA-48. Both carbapenemase genes were located on IncL/M-type conjugative plasmids. Insertion sequence IS1999 (truncated or not by IS1R) was located upstream of the bla(OXA-48) and bla(OXA-162) genes in all of the isolates. Pulsed-field gel electrophoresis typing indicated the clonal transmission of an OXA-48-producing Klebsiella pneumoniae strain in two hospitals.

Cytokine expression in the colonic mucosa of human immunodeficiency virus-infected individuals before and during 9 months of antiretroviral therapy.

High-level human immunodeficiency virus (HIV) replication and the rapid breakdown of the mucosal immune system are the hallmarks of HIV infection in the gut. Cytokine dysregulation may be related to both phenomena. Using real-time PCR we quantified the colonic mucosal mRNA expression of selected proinflammatory and regulatory (gamma interferon [IFN-gamma], tumor necrosis factor alpha [TNF-alpha], and interleukin-2 [IL-2], IL-4, IL-6, and IL-10) and HIV-inhibitory (IL-16, CCL3, and CCL5) cytokines for 10 HIV-infected patients before and during 9 months of highly active antiretroviral therapy (HAART). HIV RNA and T-cell dynamics were measured in the colonic mucosa and the blood. Seven HIV-negative individuals served as controls. The mucosal mRNA expression of TNF-alpha, IFN-gamma, IL-4, IL-6, and IL-10 was significantly higher in HIV-infected patients than in control patients and remained elevated during 9 months of HAART despite the decline in blood and mucosal HIV RNA levels and an increase in the level of CD4(+) T lymphocytes. The mRNA levels of CCL3 and CCL5, both of which were elevated before treatment, returned to nearly normal during therapy. Despite reductions in levels of mucosal HIV RNA and the restoration of mucosal CD4(+) T lymphocytes, antiretroviral therapy failed to restore the normal colonic immunologic environment.

Esophageal giant ulcer in primary human immunodeficiency virus infection is associated with an infiltration of activated T cells.

Primary human immunodeficiency virus (HIV) infection is a rarely diagnosed disease. The intestinal lymphocyte population represents a primary target of infection, virus replication, as well as cell infiltration and activation. The purpose of this study was to describe a patient suffering from esophageal giant ulcer as a clinical manifestation of primary HIV. In the present case of primary HIV infection a giant ulcer of the esophagus was diagnosed as the clinical manifestation. An upper endoscopy was performed and the biopsy specimens were further processed for immunohistochemical stainings characterizing the cellular infiltrate as well as cytokine production. In addition, seroconversion was documented and total viral load was determined. The esophageal ulceration presented the clinical manifestation of primary HIV infection since other causes of esophageal ulcerations could be excluded. The ulceration revealed an inflammatory infiltrate consisting of both CD4(+) and CD8(+) T cells. The vast majority of these cells expressed the activation marker CD38 and several cells showed interferon-gamma and interleukin-2 production. Furthermore, a substantial number of tissue infiltrating CD8(+) T cells expressed the cytotoxic molecule perforin. In addition, the HIV antigen p24 could be detected in the inflammatory infiltrate. Subsequent steroid treatment resulted in a relief of symptoms and healing of the ulcerations. These observations strongly suggest that infiltration of activated T cells plays a crucial role in the pathogenesis of giant ulcers during primary HIV infection.

Late-onset cytomegalovirus reactivation in critically ill renal transplant patients.

BACKGROUND: Cytomegalovirus (CMV) reactivation occurs frequently in the first months after renal transplantation. However, reports concerning long-term kidney transplant recipients are rare and have always pertained to symptomatic CMV disease. METHODS: We report four cases of late-onset asymptomatic CMV reactivation in critically ill renal transplant patients who suffered from severe bacterial infections and in whom CMV antigenemia was observed. RESULTS AND CONCLUSION: CMV reactivation in these patients might indicate an additional disturbance in the patients' immune defenses at the time of critical illness, possibly even necessitating a temporary reduction in immunosuppressive therapy. Prospective, controlled trials are needed to define the role of CMV antigenemia in critically ill patients, including the role of antiviral therapy for asymptomatic reactivations.

Multicenter comparison of Fungitest for susceptibility testing of Candida species.

In four laboratories the reproducibility of Fungitest, a colorimetric breakpoint method for antifungal susceptibility testing, was examined. The interlaboratory agreement of test results from 50 Candida strains was dependent on the antifungal agents and ranged from 56% to 100%. Itraconazole showed the poorest, amphotericin B and flucytosine (100% and 96%, respectively) the highest concordance. When minor discrepancies were disregarded the agreement increased to 94% to 100% for all agents. In total, major discrepancies were only seen in 2.7%. The overall agreement between concordant results and the NCCLS standard method was high, ranging between 96.4% and 100%. Generally, sensitive strains showed a better agreement with Fungitest. Since the concordance in multisite studies with Fungitest will always depend on the isolates chosen, further studies with this test are necessary.

High variability between results of different in-house tests for cytomegalovirus (CMV) monitoring and a standardized quantitative plasma CMV PCR assay.

A total of 2,718 blood samples were analyzed in five virological laboratories for the presence of cytomegalovirus (CMV) by in-house tests and one standardized plasma PCR assay. Results from in-house tests showed remarkable variability. Detection of CMV pp65 antigen or DNA from cells was more sensitive than that by plasma CMV PCR assay.