Pilot study of MRI/ultrasound fusion imaging in postpartum assessment of Cesarean section scar.

OBJECTIVE: To evaluate prospectively the uterine scar after Cesarean section (CS) and the corresponding uterine region after vaginal delivery (VD) at 6 weeks postpartum using transabdominal (TAS) and transvaginal (TVS) sonography with magnetic resonance imaging (MRI) fusion to investigate whether fusion imaging allows standardized and reproducible identification of the scar location and measurement of uterine wall thickness compared with high-resolution MRI alone. METHODS: Pelvic MRI was performed 6 weeks after delivery in 30 women (10 with planned CS (PCS), 10 with emergency CS (ECS) and 10 with VD). After transfer of MRI-DICOM datasets to the ultrasound system, the scar region after CS and the corresponding uterine region after VD were examined by TAS (5 MHz) and TVS (10 MHz) using smart fusion with MRI to guide visualization of the region in the corresponding sectional planes for both modalities. Vascularization of the scar region was determined as a percentage area using power Doppler ultrasound. Anterior (AW) and posterior (PW) uterine wall thickness was measured using TAS and TVS with fusion imaging and using MRI alone. RESULTS: TVS with fusion imaging was applied successfully for uterine assessment at the end of the postpartum period in all women. TAS failed to identify the scar area in three women. Imaging techniques were similar in the evaluation of AW and PW thickness following VD. MRI and MRI/TVS fusion showed significant differences in AW thickness or scar area, in terms of the difference relative to PW thickness, in women with PCS and ECS (MRI: PCS, 4.3 mm; ECS, 4.2 mm; VD, 0.8 mm; P = 0.034; MRI/TVS fusion: PCS, 2.0 mm; ECS, 3.3 mm; VD, 0.0 mm; P = 0.01). The degree of vascularization in the scar region measured by power Doppler ultrasound was lower after PCS (13.1 ± 9.4%/area) and ECS (17.0 ± 8.2%/area) than after VD (34.6 ± 8.5%/area; P = 0.0017). CONCLUSION: MRI/ultrasound fusion imaging can be performed in a reproducible manner for examination of the postpartum uterus. MRI/TVS fusion enables standardized identification of the CS scar location and vascularization is reduced in this area. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

Sarcocyst Development in Raccoons (Procyon lotor) Inoculated with Different Strains of Sarcocystis neurona Culture-Derived Merozoites.

Sarcocystis neurona is considered the major etiologic agent of equine protozoal myeloencephalitis (EPM), a neurological disease in horses. Raccoon ( Procyon lotor ) is considered the most important intermediate host in the life cycle of S. neurona in the United States; S. neurona sarcocysts do mature in raccoon muscles, and raccoons also develop clinical signs simulating EPM. The focus of this study was to determine if sarcocysts would develop in raccoons experimentally inoculated with different host-derived strains of in vitro-cultivated S. neurona merozoites. Four raccoons were inoculated with strains derived from a raccoon, a sea otter, a cat, and a horse. Raccoon tissues were fed to laboratory-raised opossums ( Didelphis virginiana ), the definitive host of S. neurona . Intestinal scraping revealed sporocysts in opossums who received muscle tissue from raccoons inoculated with the raccoon-derived or the sea otter-derived isolates. These results demonstrate that sarcocysts can mature in raccoons inoculated with in vitro-derived S. neurona merozoites. In contrast, the horse and cat-derived isolates did not produce microscopically or biologically detected sarcocysts. Immunoblot analysis revealed both antigenic and antibody differences when testing the inoculated raccoons. Immunohistochemical staining indicated differences in staining between the merozoite and sarcocyst stages. The successful infections achieved in this study indicates that the life cycle can be manipulated in the laboratory without affecting subsequent stage development, thereby allowing further purification of strains and artificial maintenance of the life cycle.

Severe Case of Autoimmune Thrombocytopenia First Diagnosed in Pregnancy.

We report on a 28-year old primigravida who presented in the second trimester with sudden onset of bleeding tendencies and thrombocytopenia of 2/nL during the first manifestation of autoimmune thrombocytopenia (ITP). Therapy with intravenous immunoglobulins (IVIG) and steroids was initiated but could not prevent renewed bleeding incidents and recurrent thrombocytopenia in the long term, thus premature delivery by Caesarean section in the 32 + 3 week of pregnancy could not be avoided. The bleeding complications could only be mastered by multiple thrombocyte transfusions. Because the ITP remained refractory to therapy in the postpartum period a thrombopoietin receptor agonist (TPO-RA) was administered. This led to an increase in the thrombocyte count which was later stabilised by prednisolone alone.

Sarcocystis neurona: molecular characterization of enolase domain I region and a comparison to other protozoa.

Sarcocystis neurona causes protozoal myeloencephalitis and has the ability to infect a wide host range in contrast to other Sarcocystis species. In the current study, five S. neurona isolates from a variety of sources, three Sarcocystis falcatula, one Sarcocystis dasypi/S. neurona-like isolate, and one Besnoitia darlingi isolate were used to compare the enolase 2 gene segment containing the domain I region to previously sequenced enolase genes from Neospora caninum, Neospora hughesi, Toxoplasma gondii, Plasmodium falciparum, and Trypanosoma cruzi; enolase 2 segment containing domain I region is highly conserved amongst these parasites of veterinary and medical importance. Immunohistochemistry results indicates reactivity of T. gondii enolase 1 and 2 antibodies to S. neurona merozoites and metrocytes, but no reactivity of anti-enolase 1 to the S. neurona bradyzoite stage despite reactivity to T. gondii bradyzoites, suggesting expression differences between organisms.

Development and evaluation of a Sarcocystis neurona-specific IgM capture enzyme-linked immunosorbent assay.

Equine protozoal myeloencephalitis (EPM) is a serious neurologic disease of horses caused primarily by the protozoal parasite Sarcocystis neurona. Currently available antemortem diagnostic testing has low specificity. The hypothesis of this study was that serum and cerebrospinal fluid (CSF) of horses experimentally challenged with S neurona would have an increased S neurona-specific IgM (Sn-IgM) concentration after infection, as determined by an IgM capture enzyme linked immunoassay (ELISA). The ELISA was based on the S neurona low molecular weight protein SNUCD-1 antigen and the monoclonal antibody 2G5 labeled with horseradish peroxidase. The test was evaluated using serum and CSF from 12 horses experimentally infected with 1.5 million S neurona sporocysts and 16 horses experimentally infected with varying doses (100 to 100,000) of S neurona sporocysts, for which results of histopathologic examination of the central nervous system were available. For horses challenged with 1.5 million sporocysts, there was a significant increase in serum Sn-IgM concentrations compared with values before infection at weeks 2-6 after inoculation (P < .0001). For horses inoculated with lower doses of S neurona, there were significant increases in serum Sn-IgM concentration at various points in time after inoculation, depending on the challenge dose (P < .01). In addition, there was a significant increase between the CSF Sn-IgM concentrations before and after inoculation (P < .0001). These results support further evaluation of the assay as a diagnostic test during the acute phase of EPM.