Urinary tract infection caused by carbapenem-resistant K. pneumoniae and P. aeruginosa.

There has been an increase in recent years of antimicrobial resistance of Gram negative bacilli (GNB). Carbapenems, the mainstay for the treatment of multidrug resistant GNB infections, are no longer always effective leaving treatment options limited. We present the case of patient with recurrent, complicated urinary tract infections. The current episode was caused by carbapenem-resistant K. pneumoniae and P. aeruginosa and carbapenem-susceptible, but MDR E. cloacae. Resistance to carbapenems of K. pneumoniae was conferred by the production of the class B metallo-beta-lactamase, VIM1. Infection control measures were implemented and following a 2-week course of treatment with colistin, the infection resolved and the patient was discharged. We discuss the changes in the epidemiology, the mechanisms involved and the means of detecting carbapenem resistance in GNB. We would also like to stress the role of infection control measures in limiting patient-to-patient spread of MDR organisms which, are of paramount importance in cases when few treatment options are left available.

Seven years of recurrent severe strongyloidiasis in an HTLV-I-infected man who developed adult T-cell leukaemia.

OBJECTIVE: Human T-cell leukaemia/lymphoma virus type I (HTLV-I) is endemic in Japan, the Caribbean basin and Africa, where it has been aetiologically linked to certain chronic myelopathies and adult T-cell leukamia (ATL). We sought to investigate whether strongyloidiasis, a parasitic disease common in these areas, might be a cofactor in the pathogenesis of ATL, as some reports have suggested. PATIENTS, PARTICIPANTS: One 35-year-old HTLV-I-seropositive French West Indian man with a 7-year history of recurrent strongyloidiasis associated with episodic hyperinfestation presenting at the Centre Hospitalier Intercommunal, Villeneuve St Georges, France. INTERVENTIONS: Treatment with various chemotherapeutic agents and symptomatic therapy for hypercalcaemia and antiviral therapy (zidovudine and interferon). RESULTS: The patient developed ATL and died shortly after, despite chemotherapy. Immunological and virological studies performed during the last 15 months of his life showed an increase of the percentage of peripheral ATL cells, and progression from a polyclonal to a monoclonal integration of HTLV-I proviral DNA in the peripheral blood mononuclear and lymph-node cells. CONCLUSIONS: Recurrent strongyloidiasis appears to have been a possible cofactor associated with progression from healthy carrier state to ATL in our patient.