Thirty-four consecutive patients were hospitalized with diagnosis of severe Babesia infection over the course of 13 years. The average time from onset of symptoms to diagnosis was 15 days. When compared with uninfected febrile control patients, affected patients complained significantly more often of malaise, arthralgias and myalgias, and shortness of breath (P<.05), and they more often had thrombocytopenia and abnormal liver function (P<.05). Forty-one percent of patients with Babesia developed complications such as acute respiratory failure, disseminated intravascular coagulation, congestive heart failure, and renal failure. Analysis of data revealed that complicated babesiosis was more commonly associated with the presence of severe anemia (hemoglobin level <10 g/dL; P=.01) and higher parasitemia levels (>10%; P=.08). Patients were treated with a combination of drugs that included clindamycin, quinine, atovaquone, or azithromycin. Despite treatment, parasitemia persisted for an average of 8.5 days (range, 3--21 days). Exchange transfusion was performed for 7 patients, and it effectively reduced the high levels of parasitemia. Three patients died. Improved outcomes may result with prompt recognition and treatment of babesiosis.

The survival of Salmonella montevideo during serum treatment depends on the presence of an 0 antigen (0-Ag) associated with the lipopolysaccharide molecule. In this organism, the 0 antigen is a polysaccharide composed of 0 to more than 55 subunits, each containing 4 mannose residues together with glucose and n-acetylglucosamine. We used a mutant strain of S. montevideo that smooth, enteric gram-negative bacteria is efficient, and the bactericidal C5b-9 complex is formed on the surface of such smooth cells (13). However, in contrast to the stable, hydrophobic interaction of C5b-9 with rough cells, the C5b-9 complex is bound by weak hydrophilic interactions to smooth cells and is released from the surface (14). Consequently, it is not bactericidal. We and others (13,14,36) have suggested that C5b-9 complexes are shed because complement activation takes place on long O-Ag side chains and that C5b-9 complexes formed are sterically inhibited from inserting into hydrophobic membrane domains. In a recent paper (12)

The role of glycosphingolipids as adhesion receptors for yeasts was examined. Cryptococcus neoformans, Candida albicans, and Saccharomyces cerevisiae, as well as Histoplasma capsulatum and Sporotrichum schenckii (in their yeast phases), bound specifically to lactosylceramide (GalIll-4GlcIll-lCer), as measured by overlaying glycosphingolipid chromatograms with 1251-labeled organisms. An unsubstituted galactosyl residue was

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