Lifecycle

• Intermediate host (prey) acquires infection by ingestion of sporocyst during grazing or through contaminated feed and water.
• Sporozoites are released after reaching the intestine.
• They penetrate intestinal wall and reach mesenteric lymph node, arteries.
• First generation schizonts develop in endothelial cells of small blood vessels. 2^nd generation schizonts develop in vascular endothelium of different organ/tissues including brain and spinal cord.
• Merozoites are released from these schizonts. Merozoites released from 2^nd generation initiate sarcocyst formation in straited muscle including cardiac muscles.
• These merozoites first become round to avoid. After repeated asexual division, sarcocyst is filled with crescent shaped bradyzoites which become infective stages on maturation.
• Definitive host acquire infection after ingestion of meal of infected host.
• Bradyzoites are liberated in stomach and intestine. Bradyzoites move actively and penetrate muscosa of small intestine, where they transform to male and female gamonts.
• Macrogamonts are ovoid to round and contain single nucleus. Mature microgamonts are ovoid to elongate and contain microgametes.
• Macrogamete and microgamete fertilize and wall develops around zygote and oocyst is formed.
• Oocyst sporulate in lamina proprid. Sporulated oocyst are then passed out in faceces from which intermediate host gets infection.
• Gametogonic stages develop either in goblet cells at or near the surface of intestine or in enterocysts next to basement membrane adjoining lamina propria or rarely in mesenteric lymph node.
• Because of asynchronous sporulation and cyst wall being membranous, few sporulated oocyst appear in the beginning in faeces followed by discharge of sporocysts for a long period patency.

Mode of transmission

• Transmission in intermediate host is through ingestion of contaminated feed or water.
• Transmission in final host is through ingestion of contaminated meat.

Clinical signs/ Pathogenesis

a. Sarcocystis cruzi (cattle, other species included)

• Fever, Anorexia, Loss of weight, Hair loss, Weakness, Neurological signs and death.
• Muscle twitching, prostration, abortion, reduced milk yield, Hypersalivation.

b. S. tenella (Sheep, other species included)

• Anorexia, Weight loss, fever, Anemia, Loss of wool.
• Abortion, Premature birth, Nervous signs, Myositis, Death.

c. S. capracanis (goat, inckude other species infecting goat)

• Most pathogenic in goats
• Fever, Weakness, Anorexia, Weight loss, Tremors
• Irritability, Abortion and Death.

Sarcocystiosis in Pig

• Three species reported from pigs; miescheriana, S. scichominis, S. porcifelis.
• Clinical signs include weight loss, purpura of skin of ear and buttocks, Dyspnoea, Muscle tremors, Abortion and death.

Sarcocystiosis in Equines

• Four species ; bertami, S. equicanis, S. fayeri and S. asinus
• Clinical signs include anemia, Anorexia, Fever, Excessive salivation, Abortion and Loss of body hair.

Diagnosis

• On the basis of clinical signs.
• Demonstration of sporulated oocyst in feces of definitive host.
• Defection of Ab in serum can help in diagnosis of acute sarcocystiosis. ELISA is used in detection of circulating antigen in mice.

Treatment

• Most of anticoccidials drugs; Amprolium, Salinomycin works.

Prevention and control

• Interruption of life-cycle to minimize spread of sporocyst shed by definitive host. It can be bought by:

1. Keeping away carnivorous from animal houses and from their food, water and bedding.
2. Uncooked meat should never be fed to carnivorous.
3. Dead animals should be buried or incinerated to avoid access to carnivorous.
4. Feeding freeze dried meat or cooking meat at 55⁰C for 20 minutes can kill sarcocyst in meat.