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Opossum protein neutralizes nearly all poisons, could have benefits for humans
Opossums may someday provide an antidote to nearly all forms of poison, including everything from snakebites to ricin.
The Journal of Venomous Animals and Toxins has found that the American opossum produces a protein known as Lethal Toxin-Neutralizing Factor (LTNF). And as the Boing Boing blog points out, the LTNF protein is exactly what it sounds like, seeking out otherwise lethal poisons that have entered an opossum's body and neutralizing them.
Link: http://www.novamir.org/
Sounds perfectly plausible, though the story goes on to explain that this journal article was first published in 1999... seems like a big delay if the news is this remarkable. 
3 replies
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= new reply since forum marked as read
It's pretty devastating for horses that get it - they become uncoordinated and treatment is prolonged and expensive. If very much damage has already been done to the nervous system, full recovery is improbable.
Parasite
Sarcocystis neurona is the most common cause of equine protozoal myeloencephalitis (EPM) in horses in America. It is a single celled parasite belonging to the group called coccidia (Apicomplexa: Sarcocystidae) with opossums as the definitive hosts and a variety of mammals as aberrant or natural intermediate hosts . Only asexual stages have been identified in the aberrant intermediate hosts, and they are confined to the brain and spinal cord, and any part of the central nervous system (CNS) may be affected. In histologic sections of CNS, individual merozoites are about 3-5 um long and contain a single, centrally located vesicular nucleus. The sarcocysts are microscopic (~700 um long) with a 1-3 um thick sarcocyst wall. The bradyzoites are slender and tiny (~ 5 um long). Sarcocystis neurona sporocysts from opossum faeces are ~ 10 x 8 um in size.
Life Cycle
It has the most unusual life cycle for any species of Sarcocystis as unlike other species of Sarcocystis, S. neurona has wide host range for its intermediate hosts. Opossums (Didelphis virginiana, D. albiventris) are its definitive (reservoir) hosts and excrete oocysts and sporocysts (environmentally resistant stage)in their feces. Raccoons, armadillos, sea otters, skunks, cats and possibly other mammals are intermediate hosts. These animals ingest the sporocysts , which after many asexual cycles, lead to the development of sarcocysts (resting stage) in their muscles. Infection of the final host is by the ingestion of the sarcocysts from the muscles of the intermediate hosts. The bradyzoites are released in the intestines of the definitive host. They undergo a sexual cycle and this ultimately result in the production of sporulated oocysts, which are excreted in the feces of the opossum. Horses are considered its aberrant hosts because only schizonts and merozoites (no sarcocysts) have been identified , confined to the brain and spinal cord.
Clinical Disease
The pathogenesis of EPM is not clear because the complete life cycle is unknown. Sarcocystis neurona can parasitize all regions of the CNS, from the anterior cerebrum to the end of the spinal cord. Sarcocystis neurona schizonts and merozoites are found in neurons, mononuclear cells, glial cells, and perhaps other neural cells. Studies in immune deficient, interferon gamma gene knockout (KO) mice fed S. neurona sporocysts indicate that S. neurona initially multiplies to a limited extent in visceral tissues and then is transported to the CNS probably via leukocytes. Three weeks after infection, S. neurona is mainly confined to the CNS. Clinical signs of EPM are dependent on the area of the CNS parasitized. The early clinical signs of stumbling and frequent interference are often easily confused with a lameness of either the thoracic and/or the pelvic limbs. In many horses the disease tends to have a gradual progression of clinical signs including ataxia, but in some horses there may be mild clinical signs followed by a rapidly progressive course. On physical examination, the vital signs are usually normal, although some horses may appear thin and mildly depressed. Neurological examination often reveals an asymmetric weakness, ataxia and spasticity involving all 4 limbs. Frequently, areas of hypalgesia or complete sensory loss may be noted. The most frequent brain or cranial nerve deficits observed in horses appear to be head tilt, depression, facial nerve paralysis, and difficulty swallowing, although signs are not limited to these areas. Gait abnormalities are often a result of damage to the spinal cord and may be quite variable depending on the location and severity of the lesion.
http://www.ars.usda.gov/main/docs.htm?docid=11028
Sarcocystis neurona is the most common cause of equine protozoal myeloencephalitis (EPM) in horses in America. It is a single celled parasite belonging to the group called coccidia (Apicomplexa: Sarcocystidae) with opossums as the definitive hosts and a variety of mammals as aberrant or natural intermediate hosts . Only asexual stages have been identified in the aberrant intermediate hosts, and they are confined to the brain and spinal cord, and any part of the central nervous system (CNS) may be affected. In histologic sections of CNS, individual merozoites are about 3-5 um long and contain a single, centrally located vesicular nucleus. The sarcocysts are microscopic (~700 um long) with a 1-3 um thick sarcocyst wall. The bradyzoites are slender and tiny (~ 5 um long). Sarcocystis neurona sporocysts from opossum faeces are ~ 10 x 8 um in size.
Life Cycle
It has the most unusual life cycle for any species of Sarcocystis as unlike other species of Sarcocystis, S. neurona has wide host range for its intermediate hosts. Opossums (Didelphis virginiana, D. albiventris) are its definitive (reservoir) hosts and excrete oocysts and sporocysts (environmentally resistant stage)in their feces. Raccoons, armadillos, sea otters, skunks, cats and possibly other mammals are intermediate hosts. These animals ingest the sporocysts , which after many asexual cycles, lead to the development of sarcocysts (resting stage) in their muscles. Infection of the final host is by the ingestion of the sarcocysts from the muscles of the intermediate hosts. The bradyzoites are released in the intestines of the definitive host. They undergo a sexual cycle and this ultimately result in the production of sporulated oocysts, which are excreted in the feces of the opossum. Horses are considered its aberrant hosts because only schizonts and merozoites (no sarcocysts) have been identified , confined to the brain and spinal cord.
Clinical Disease
The pathogenesis of EPM is not clear because the complete life cycle is unknown. Sarcocystis neurona can parasitize all regions of the CNS, from the anterior cerebrum to the end of the spinal cord. Sarcocystis neurona schizonts and merozoites are found in neurons, mononuclear cells, glial cells, and perhaps other neural cells. Studies in immune deficient, interferon gamma gene knockout (KO) mice fed S. neurona sporocysts indicate that S. neurona initially multiplies to a limited extent in visceral tissues and then is transported to the CNS probably via leukocytes. Three weeks after infection, S. neurona is mainly confined to the CNS. Clinical signs of EPM are dependent on the area of the CNS parasitized. The early clinical signs of stumbling and frequent interference are often easily confused with a lameness of either the thoracic and/or the pelvic limbs. In many horses the disease tends to have a gradual progression of clinical signs including ataxia, but in some horses there may be mild clinical signs followed by a rapidly progressive course. On physical examination, the vital signs are usually normal, although some horses may appear thin and mildly depressed. Neurological examination often reveals an asymmetric weakness, ataxia and spasticity involving all 4 limbs. Frequently, areas of hypalgesia or complete sensory loss may be noted. The most frequent brain or cranial nerve deficits observed in horses appear to be head tilt, depression, facial nerve paralysis, and difficulty swallowing, although signs are not limited to these areas. Gait abnormalities are often a result of damage to the spinal cord and may be quite variable depending on the location and severity of the lesion.
http://www.ars.usda.gov/main/docs.htm?docid=11028
