Prevalence of agglutinating antibodies to Sarcocystis neurona in raccoons, Procyon lotor, from the United States

Equine protozoal myeloencephalitis (EPM) is the most important protozoal disease of horses in North America and it is caused by Sarcocystis neurona. Natural cases of encephalitis due to S. neurona have been reported in raccoons, Procyon lotor. We examined 99 raccoons for agglutinating antibodies to S. neurona using the S. neurona agglutination test (SAT) employing formalin-fixed merozoites as antigen. Raccoons originated in Florida (N=24, collected in 1996), New Jersey (N=25, collected in 1993), Pennsylvania (N=25, collected in 1999), and Massachusetts (N=25, collected in 1993 and 1994). We found that 58 (58.6%) of the 99 raccoons were positive for antibodies to S. neurona using the SAT; 44 of 99 raccoons (44%) had titers of ≥1:500. This prevalence is similar to the reported seroprevalence of 33–60% for S. neurona antibodies in horses from the United States using the Western blot test.     

住肉孢子虫病检疫技术概述

住肉孢子虫病是由住肉孢子虫引起的一种原虫病,本病发生于各种家畜（马、牛、羊、猪、兔等）、鼠类、鸟类、爬虫类和鱼类中,偶尔也寄生于人。我国各地的牛羊,尤其是南方的水牛和黄牛、北方的绵羊和山羊常有发现,有些地区的感染率可达100%。住肉孢子虫寄生于各种家畜的横纹肌,致使肌肉不能食用,引起巨大的经济损失。本文对住肉孢子虫病的产地检疫技术、屠宰检疫技术和实验室检疫技术作以简要介绍。     

家畜住肉孢子虫感染情况调查

对北京,河北,内蒙,云南,湖南等地家畜住肉孢子虫的感染情况进行了调查,黄牛,水牛,绵羊,山羊和猪的平均感染率分别为４３．５％、９１％、５６．６％、５９．６％和１３．８％。调查还发现,同一畜种不同地方的感染率有着明显差异。在不同饲养方式下对住肉孢子虫的感染率也明显不同。     

水牛枯氏住肉孢子虫在水牛与黄牛体内的发育史

11头5～8月龄公水牛犊和2头7日龄黑白花奶牛犊,分别人工感染80～2000万个水牛源枯氏住肉孢子虫孢子囊,2头同龄公水牛犊不感染作对照。感染后12、22和32天在大、中、小血管和毛细血管内出现第一代裂殖体,32.86×16.43(19.08～46.64×12.72～21.2)μm,含100～450个裂殖子;32～46天在毛细血管和小血管内发现大量的第二代裂殖体,18.21×9.87(10.60～29.68×6.36～13.78)μm,含30～110个裂殖子;28～40天,第二代裂殖子出现于血液中或单核细胞内;46天初级幼包囊形成,78天部分包囊成熟,98天(黄牛)包囊成熟。     

Sarcocystis calchasi encephalitis in a rock pigeon

A rock pigeon (Columba livia) caught in Akihabara, Tokyo, showed neurological symptoms, such as head tilt and circling. Pathological examinations revealed abundant Sarcocystic cysts in the skeletal muscle and myocardium with mild myositis, and numerous schizonts and sarcocysts with severe multifocal granulomatous T-lymphocytic infiltration in the central nervous system. A Sarcocystis calchasi-specific gene was detected in the muscle and brain. This case indicates S. calchasi was distributed in Japan and caused severe encephalitis to rock pigeons.     

Molecular characterization of Sarcocystis spp. as a cause of protozoal encephalitis in a free-ranging black bear

A free-ranging juvenile male black bear (Ursus americanus), found dead in Alberta, Canada, had severe nonsuppurative encephalitis. Lesions in the brain were most severe in the gray matter of the cerebral cortex, and included perivascular cuffs of lymphocytes and plasma cells, areas of gliosis that disrupted the neuropil, and intralesional protozoan schizonts. The left hindlimb had suppurative myositis associated with Streptococcus halichoeri. Immunohistochemistry and molecular analyses (PCR and sequencing of 4 discriminatory loci: 18S rDNA, ITS-1 rDNA, cox1, rpoB) identified Sarcocystis canis or a very closely related Sarcocystis sp. in the affected muscle and brain tissues. The main lesion described in previously reported cases of fatal sarcocystosis in bears was necrotizing hepatitis. Fatal encephalitis associated with this parasite represents a novel presentation of sarcocystosis in bears. Sarcocystosis should be considered a differential diagnosis for nonsuppurative encephalitis in bears.     

Prevalence of Sarcocystis neurona and Neospora spp. infection in horses from Brazil based on presence of serum antibodies to parasite surface antigen

Sera from 961 horses from Brazil were tested for antibodies against the major surface antigens SnSAG4 and NhSAG1 to determine the seroprevalence of Sarcocystis neurona and Neospora hughesi, respectively. Antibodies against SnSAG4 were detected in 669 (69.6%) of the horses, while antibodies against NhSAG1 were detected in only 24 (2.5%) of the horses. These serologic results suggest that there is a high concentration of S. neurona in the environment of Brazil, which results in marked exposure of horses to this parasite. Additionally, the data further confirm that infection with Neospora spp. is relatively uncommon in horses.     

Fatal hepatic sarcocystosis in a puppy with eosinophilia and eosinophilic peritoneal effusion

A 3-month-old male Golden Retriever puppy was evaluated for lethargy and fever of 2-days duration. Results of a CBC and biochemical profile revealed marked eosinophilia (6.3 X 10(3)/microL; reference interval 0.1-1.2 X 10(3)/microL), moderate thrombocytopenia, and increased activities of alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Hepatomegaly and peritoneal effusion were found using abdominal ultrasound. Peritoneal fluid analysis revealed eosinophilic inflammation (23,000 nucleated cells/microL with 88% eosinophils). Despite supportive treatment the puppy's condition deteriorated rapidly; euthanasia was requested, and a necropsy performed. Microscopically, there was marked necrosuppurative and eosinophilic hepatitis with vasculitis. Numerous hepatocytes contained protozoal organisms suspected to be Toxoplasma gondii or Neospora caninum. However, serum was negative for both T gondii and N caninum antibodies; polymerase chain reaction assay on hepatic tissue was negative for both organisms; and immunohistochemical evaluation of hepatic tissue using serum raised against T gondii, N caninum, and Sarcocystis neurona also was negative. Schizont morphology suggested that merozoites replicated by endopolygeny, forming rosettes around a central residual body. Transmission electron microscopy revealed that merozoites lacked rhoptries. These findings were consistent with a diagnosis of Sarcocystis canis, an apicomplexan parasite with an unknown life cycle.