Disseminated Bipolaris spicifera in a neonate.

We report a premature infant with disseminated fungal infection identified as Bipolaris spicifera. The infant was born at 23 4/7 weeks' gestation, weighing 780 g. At day of life (DOL) 7 erythematous areas on the back were noticed that progressed to black, necrotic skin lesions. A shave biopsy showed invasive fungal organisms that were identified by culture as B. spicifera. The lesions progressed despite aggressive surgical debridement and antifungal therapy. On autopsy, fungal organisms found throughout the internal organs confirmed disseminated disease with B. spicifera. This organism is now more often recognized as a human pathogen; however, this is the first reported case in a neonate.

Eradication of Cryptosporidium in a child undergoing maintenance chemotherapy for leukemia using high dose azithromycin therapy.

PURPOSE: To describe a case of severe diarrhea caused by Cryptosporidium in a patient undergoing maintenance chemotherapy. Important aspects of disease caused by Cryptosporidium, including diagnosis and treatment, are also reviewed. METHODS AND RESULTS: A 4-year-old boy with acute lymphoblastic anemia in remission had a prolonged course of diarrhea and wasting. C. parvum was identified in the gastrointestinal tract by biopsy and in the stool using modified acid fast staining. Improvement in the stool consistency was noted after 3 days of therapy with azithromycin, and, after 14 days of therapy, Cryptosporidium oocysts could no longer be identified in the stool. CONCLUSIONS: C. parvum should be considered in all immunocompromised patients with severe or prolonged diarrhea, especially if there is no blood or leukocytes in the stool. Because Cryptosporidium is not always tested for in a routine ova and parasite examination, the lab should be notified if it is in the differential diagnosis. Azithromycin therapy may prove beneficial in the treatment of intestinal Cryptosporidium in immunocompromised individuals.

Threonine-89 participates in the active site of bacteriorhodopsin: evidence for a role in color regulation and Schiff base proton transfer.

Bacteriorhodopsin (bR) functions as a light-driven proton pump in the purple membrane of Halobacterium salinarium. A major feature of bR is the existence of an active site which includes a retinylidene Schiff base and amino acid residues Asp-85, Asp-212, and Arg-82. This active site participates in proton transfers and regulates the visible absorption of bacteriorhodopsin and its photointermediates. In this work we find evidence that Thr-89 also participates in this active site. The substitution Thr-89 --> Asn (T89N) results in changes in the properties of the all-trans retinylidene chromophore of light-adapted bR including a redshift of the visible lambda(max) and a downshift in C=N and C=C stretch frequencies. Changes are also found in the M and N intermediates of the T89N photocycle including shifts in lambda(max), a downshift of the Asp-85 carboxylic acid C=O stretch frequency by 10 cm(-1), and a 3-5-fold decrease in the rate of formation of the M intermediate. In contrast, the properties of the 13-cis retinylidene chromophore of dark-adapted T89N as well as the K and L intermediates of the T89N photocycle are similar to the wild-type bacteriorhodopsin. These results are consistent with an interaction of the hydroxyl group of Thr-89 with the protonated Schiff base of light-adapted bR and possibly the N intermediate but not the 13-cis chromophore of dark-adapted bR or the K and L intermediates. Thr-89 also appears to influence the rate of Schiff base proton transfer to Asp-85 during formation of the M intermediate, possibly through an interaction with Asp-85. In contrast, the hydroxyl group of Thr-89 is not obligatory for proton transfer from Asp-96 to the Schiff base during formation of the N intermediate.

Asp 46 can substitute Asp 96 as the Schiff base proton donor in bacteriorhodopsin.

Bacteriorhodopsin functions as a light-driven proton pump in the purple membrane of Halobacterium salinarium. A variety of studies have established that a proton is transferred over an approximately 10 A distance from Asp 96 to the retinylidene Schiff base during the M --> N transition of the bR photocycle. In order to further explore the mechanism of this Schiff base reprotonation, we compared the properties of the double mutant Thr 46 --> Asp/Asp 96 --> Asn (T46D/D96N), the single mutants Asp 96 --> Asn (D96N) and Thr 46 --> Asp (T46D), and wild-type bR. In contrast to D96N, which exhibits a very slow M decay, T46D/D96N has an M decay close to that of wild-type bR. FTIR difference spectroscopy detects bands in the carboxyl and carboxylate stretch region of T46D/D96N consistent with the deprotonation of Asp 46 during the M --> N transition. In addition, bands associated with structural changes of Asn 96 in the mutant D96N are absent in T46D/D96N. Resonance Raman spectroscopy provides evidence that both T46D/D96N and T46D have a long-lived N-like species in their photocycles. These data demonstrate that Asp 46 can substitute for Asp 96 as the proton donor group in the reprotonation pathway of the Schiff base during the M --> N transition. However, N decay is delayed in comparison to wild-type bR. This may be due to a partial block in the proton pathway leading from the cytoplasmic medium to Asp 46.

Nonhematopoietic gastrointestinal neoplasia in cats: a retrospective study of 44 cases.

Gastrointestinal neoplasms other than lymphosarcomas and mast cell tumors were diagnosed in 44 cats during a 14-year period at the Washington Animal Disease Diagnostic Laboratory. All the tumors were malignant; 31 metastasized or recurred. One cat had fibrosarcoma; another, leiomyosarcoma. The other 42 cats had adenocarcinomas, which were subclassified into three histologic patterns: tubular adenocarcinoma; undifferentiated carcinoma; and mucinous adenocarcinoma. The cats averaged 10.6 years of age. There was no sex predisposition. Siamese cats had a higher frequency of adenocarcinomas than other breeds. Osseous and chondroid metaplasia occurred in nine adenocarcinomas.