Intestinal protozoa are becoming increasingly recognized as significant pathogens in immunocompromised hosts. However, pathogenesis of infection is still poorly understood, diagnostic tests remain insensitive, and management continues to pose a challenge. Invasion by intestinal protozoa can be facilitated by impaired host T-cell immune response, although the exact pathogenesis at the cellular level is unclear. HIV-infected and transplant patients have been reported to have the highest risk for developing severe disease. Cryptosporidium is the most common parasite encountered in the immunocompromised host, followed by Cyclospora and Isospora. In recent years, Microsporidia and Blastocystis have also emerged as important players, due in part to improved molecular diagnostic assays. Effective drugs against these parasites in immunocompromised patients have not been reported in recent years. When possible, reducing the level of immunosuppression seems to be the most effective treatment strategy in combination with adjunctive antiparasitic therapy. Despite that intestinal protozoan infections cause greater morbidity and mortality in the immunocompromised host, their pathogenesis in the setting of immunosuppression is poorly understood and efforts to develop new therapeutic agents are rather limited. Improving detection and identification of species or subtypes by PCR will result in improved management decisions and a better understanding of the epidemiology of intestinal protozoa. Favorable clinical outcomes can be achieved by early detection and effective treatment of the infection. Further research on key aspects of pathogenesis at the cellular level in humans is needed.

To describe the tolerance to long-term telavancin therapy among inpatients as it relates to nephrotoxicity. Retrospective cohort study of adult patients who received telavancin at the Barnes-Jewish Hospital from 1 September 2009 to 1 December 2010. Patients who received less than three doses of telavancin, were on haemodialysis prior to telavancin administration or died within 48 h of initial telavancin administration were excluded. Twenty-one patients received telavancin and met the inclusion criteria. Seven of 21 patients (33%) developed acute renal insufficiency during therapy. Patients who developed acute renal insufficiency had a mean glomerular filtration rate reduction of 56 mL/min/1.73 m². In the univariate analysis, high body mass index (P = 0.025), use of intravenous contrast dye (P = 0.017) and prior serum vancomycin trough levels >20 mg/L (P = 0.017) were associated with developing acute renal insufficiency. Two patients required haemodialysis; two had persistent renal insufficiency. Supratherapeutic vancomycin trough levels, high body mass index and receipt of intravenous contrast dye prior to telavancin therapy were associated with acute renal insufficiency.