In vitro cultivation of Sarcocystis neurona from the spinal cord of a horse with equine protozoal myelitis.
Abstract: Asexual stages of Sarcocystis neurona were seen in cultured bovine monocytes (M617) inoculated with tissue homogenates from the spinal cord of a horse with naturally acquired protozoal myelitis. Organisms first were observed as intracytoplasmic schizonts and later as motile extracellular zoites capable of infecting surrounding M617 cells. Parasites most often occurred as clusters of merozoites dispersed throughout the host cell cytoplasm; however, schizonts also contained merozoites arranged in a radial fashion surrounding a prominent residual body. Schizonts divided by endopolygeny. The parasite has been maintained beyond 280 days in the laboratory by serial passage of infected M617 cells.
Publication Date: 1991-10-01 PubMed ID: 1919932
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- Journal Article
Summary
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This research investigates the in vitro growth of the parasite Sarcocystis neurona, associated with a disease in horses known as equine protozoal myelitis, using a tissue sample from the spinal cord of an infected horse. The parasite was effectively cultivated and maintained in a lab environment for more than 280 days.
Objective and Key Findings
- The major objective of the study was to characterize the growth and development of the parasite Sarcocystis neurona in vitro, or in a controlled lab environment.
- The parasites were cultured from the spinal cord of a horse with naturally acquired protozoal myelitis, a neurologic disease characterized by inflammation and damage to the horse’s spinal cord.
- Using bovine monocytes, a type of immune cell found in the blood, the team could replicate the life cycle stages of the parasite. First, they were seen as intracytoplasmic schizonts and later as motile extracellular zoites.
- The researchers reported that the parasites most frequently appeared as clusters of merozoites inside the host cell cytoplasm. In some cases, the merozoites surrounded a noticeable residual body in a radial pattern within the schizonts.
- It was found that these schizonts divided through a process called endopolygeny, where one parent cell gives rise to several daughter cells simultaneously.
- The researchers were successful in maintaining the cultured parasites for more than 280 days by serial passage of infected monocyte cells, indicating the method’s effectiveness and potential for use in further research.
Implications of the Research
- This study offers a novel method to culture and maintain Sarcocystis neurona, providing a foundation for subsequent research focusing on this parasite and related diseases.
- Understanding the parasite’s life cycle and development in a lab setting may lead to the development of more effective prevention and treatment strategies against equine protozoal myelitis.
- This in vitro method reduces the need for live horse models, promoting more ethical research practices.
- Further, the research holds potential in narrowing the knowledge gap in the basic biology of this specific parasite and may support drug discovery and vaccine development efforts.
Cite This Article
APA
Davis SW, Speer CA, Dubey JP.
(1991).
In vitro cultivation of Sarcocystis neurona from the spinal cord of a horse with equine protozoal myelitis.
J Parasitol, 77(5), 789-792.
Publication
Researcher Affiliations
- Zoonotic Diseases Laboratory, U.S. Department of Agriculture, Beltsville, Maryland 20705.
MeSH Terms
- Animals
- Cell Line
- Horse Diseases / parasitology
- Horses
- Monocytes / parasitology
- Myelitis / parasitology
- Myelitis / veterinary
- Sarcocystis / growth & development
- Sarcocystosis / parasitology
- Sarcocystosis / veterinary
- Spinal Cord / parasitology
Citations
This article has been cited 2 times.- Morris EK, Smith NG. Bibliographic processes and products, and a bibliography of the published primary-source works of B. F. Skinner.. Behav Anal 2003 Spring;26(1):41-67.
- Liang FT, Granstrom DE, Zhao XM, Timoney JF. Evidence that surface proteins Sn14 and Sn16 of Sarcocystis neurona merozoites are involved in infection and immunity.. Infect Immun 1998 May;66(5):1834-8.
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