The quenching of the luminescence of the uranyl ion by other metal ions has been studied in aqueous solution. The quenching is shown to be a dynamic process, and the correlation of the logarithm of the quenching rate with the metal ion ionization potential suggests that intermolecular electron transfer is the predominant mechanism. Evidence that this involves complete electron transfer comes from flash photolysis of solutions of UO:' and manganese(n), where a broad absorption (Amax = 505 nm) is observed which is assigned to Mn3+. Consideration of the energetics of the quenching process suggests that in the quenching of uranyl by silver@, the products (UO: and AS"+) are produced in their electronic ground states. Studies of the effect of temperature on the quenching suggest that if an intermediate complex (exciplex) is involved in the quenching then this must involve only very weak binding. With siiver(I), the quenching is sensitive to the ionic strength of the solution. Further studies suggest that the lifetime of the luminescent state of the uranyl ion in aqueous solution varies with both temperature and uranyl ion concentration.

Miltefosine is the first effective oral drug against visceral leishmaniasis. However, there are few data about its role against the increasing problem of HIV-associated visceral leishmaniasis. It is necessary to establish a treatment and secondary prophylaxis approach with miltefosine in this population, particularly for those in whom standard treatment was unsuccessful. We report our experience with miltefosine in 5 HIV-infected patients. Miltefosine was used in relapse treatments (50 mg, b.i.d.) in 3 patients and as maintenance therapy (50 mg, 3 times/week) in all of them. Miltefosine was discontinued after full recovery of immune function in 4 patients. The median disease-free period has been 20 months since miltefosine discontinuation. One patient was lost to follow-up. Miltefosine dosage regimens for the treatment of relapses and for maintenance treatment in HIV-infected patients should be established in prospective studies.

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Whipple disease is a rare, chronic multisystem infectious disease. The central nervous system (CNS) is secondarily involved in 43% of patients; 5% of patients have isolated or primary CNS involvement. The most frequent CNS symptoms are cognitive changes. Prosopagnosia is an inability to recognize familiar faces, in a person who does not have vision impairments or cognitive alterations. This relatively rare condition is usually related to vascular, traumatic, degenerative, or infectious lesions. We report a 54-year-old woman who presented subacutely with fever, headache, and seizures that led to a diagnosis of infectious meningoencephalitis. She improved temporarily on broad-spectrum antibiotics, but then developed a chronically evolving cognitive impairment with associative prosopagnosia as the major complaint. She had a history of sporadic abdominal pain and mild sacroiliac arthralgia. After a negative duodenal biopsy, we confirmed primary CNS Whipple disease by polymerase chain reaction and brain biopsy. We treated the patient with ceftriaxone for 15 days and then co-trimoxazole for 2 years. At 8-year follow-up, she had no further impairments, but continuing prosopagnosia. To our knowledge, this is the first description of isolated prosopagnosia in a patient with primary CNS Whipple disease. Because CNS Whipple disease can lead to serious, irreversible lesions if not promptly treated, clinicians must suspect the diagnosis, treat with long-term antibiotics, and follow patients carefully to prevent recurrence.

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