Synonyms: Sarcocystis besnoiti, Gastrocystis robini, Gastrocystis besnoiti, Globidium besnoiti. The nomenclature of this species has been discussed by Jellison (1956).
Disease: Besnoitiosis, olifantvel.
Hosts: Cattle. Pols (1954) infected the domestic rabbit experimentally.
Location: The cysts are in the cutis, subcutis, connective tissue, fascia, serosae, mucosae of the nose, larynx and trachea, and other places. Trophozoites are in the blood, either extracellularly or in monocytes, and in smears of lymph nodes, lungs, testes, etc.
Geographic Distribution: Europe (southern France, Pyrenees, Portugal), Africa (South Africa, Belgian Congo, Angola, Sudan).
Prevalence: According to Hofmeyr (1945), B. besnoiti is endemic in South Africa thruout the whole of the Bushveld area from the Western Transvaal to Potgietersrust district and probably further north. Herin (1952) found it in about 2% of the cattle he examined in Ruanda-Urundi, Belgian Congo. Leitao (1949) discussed its occurrence in Portugal.
Morphology: The pseudocysts are more or less spherical, without septa, and about 100 to 500 u in diameter. The pseudocyst wall is composed of a thin inner layer containing several flattened, giant nuclei and a thick, homogeneous or concentrically laminated outer wall. The trophozoites in the pseudocysts are crescentic or banana-shaped, with 1 end pointed and the other rounded. According to Pols (1954) the trophozoites in blood, lung and testis smears of experimentally infected rabbits measure 5 to 9 by 2 to 5 u and are usually elongate oval and slightly pointed at one end. Banana-shaped and crescentic forms are found more rarely. The nucleus is more or less central.
Life Cycle: The natural mode of transmission is unknown, but it is probably thru ingestion. Hofmeyr (1945) gave circumstantial evidence that the infection is spread thru contaminated watering troughs in South Africa. Jellison, Fullerton and Parker (1956) transmitted the related B. jellisoni to house mice by feeding trophozoites from cysts of infected deer-mice or from peritoneal fluid of infected house mice.
Cuille and Chele (1937), Barrairon (1938) and Pols (1954) transmitted B. besnoiti to cattle by intravenous injection of blood from cattle in the primary stage of the disease. Pols also infected an ox by intraperitoneal injection and rabbits by intravenous, intraperitoneal and subcutaneous injection of blood. He passed the protozoon from a rabbit thru 2 generations of cattle and back to a rabbit. Later (1954a) he reported having passed it thru 19 serial passages in the rabbit. He was unable to infect mice, rats and guinea pigs.
The incubation period in the cattle infected by Pols varied from 6 to 10 days, and that in the rabbits from 6 to 16 days. It was followed by a thermal reaction which lasted 2 to 5 days. Cysts were found in the skin of naturally and artificially infected cattle 6 to 28 days after the beginning of the temperature reaction.
Pols (1954a) described cyst formation in experimentally infected rabbits. The initial stages were seen as early as 16 to 18 days after inoculation. When a trophozoite invades a histiocyte, a vacuole is formed around it. The trophozoites in tissue sections measure about 3 by 1.5 u, and the vacuoles are about 8 u in diameter. The trophozoites multiply by binary fission; Pols saw a few cases of multiple fission but they were so rare that he considered them aberrant. It is possible that the trophozoites may actually divide by endodyogeny, since Goldman, Carver and Sulzer (1958) stated that this takes place in B. jellisoni.
The nucleus of the host cell begins to divide at the same time that the trophozoites do, forming a multinucleate cell. As the parasites multiply within the vacuole, the latter becomes larger and the host cell cytoplasm is compressed to form a narrow rim. This is the middle layer of the pseudocyst wall. Within it is an inner membrane which can be seen only if 2 trophozoites have invaded the same host cell, in which case it forms a thin line between the resultant cysts; it is uncertain whether it is formed by the parasite, the host or both. Concentric layers of collagenous fibers are laid down around the host cell to form a hyaline capsule around the whole; this is the outer layer of the pseudocyst.
Pathogenesis: The most complete description of bovine besnoitiosis has been given by Hofmeyr (1945). He found it in cattle of all ages from 6 months up. Aged animals were also affected. He recognized 3 stages in the course of the disease:
The febrile stage. The first sign of besnoitiosis is fever, up to 107° F but usually lower. The animal develops a photophobia and stays in the shade. The hair loses its luster, especially along the buttocks, limbs, flanks, lower abdomen and neck. Marked anasarca develops, especially along the lower line but sometimes over the whole body. The swellings are warm and tender. The animals have a stiff gait and are reluctant to move. The pulse is fast, respiration is rapid, and rumination decreases or ceases. Diarrhea is sometimes present, and abortions are not uncommon. The lymph nodes, especially the prescapular and precrural ones, are enlarged. Lachrymation and hyperemia of the sclera are present. The cornea is studded with whitish, elevated specks which are Besnoitia cysts. The nasal mucosa becomes bright red and is also studded with cysts. The mucosa may be swollen and there may be a rapidly progressive rhinitis; it starts with a mucous discharge which later becomes thick, hemorrhagic and mucopurulent, forming dark brown crusts in the nostrils. If the pharynx and larynx are involved, there is a short cough. This stage may last 5 to 10 days. The acute stage then subsides and the second stage begins.
The depilatory stage. In this stage, the pathologic and clinical pictures are dominated by skin lesions. The skin becomes greatly thickened and loses its elasticity. The hair falls out over the swollen parts, and the skin on the flexor surfaces cracks and a sero-sanguinous fluid oozes out. Necrosis of the skin develops on the parts in contact with the ground when the animal lies down. Toward the end of this stage, hard sitfasts develop on the sides of the stifles, brisket and elbows. The anasarca subsides, leaving the skin with typical, broad wrinkles along the lower line. The photophobia decreases, and grazing is resumed in many cases. Death may occur at this stage. If not, the stage lasts 2 weeks to about a month and gradually passes into the third stage.
The seborrhea sicca stage. In this stage, most of the hair on the previously anasarcous skin has been lost, and the denuded parts are covered by a thick, scurfy layer. The sitfasts crack away from the underlying tissues, fissures remain in the flexor surfaces, the skin hardens, and deep scars show plainly. The hide resembles that of an elephant, and the animal looks as tho it has mange. The lymph nodes are permanently enlarged, the protozoan cysts remain, and the animal is listless and debilitated.
In light infections in which there has been little hair loss, the animals become practically normal in appearance, but in more severe cases recovery requires months or even years, and the changes in the cutis and subcutis and the loss of most of the hair are permanent. In convalescent animals the remaining hair forms patterns resembling the markings on a giraffe. The morbidity in a herd varies from 1 to 20%, and the mortality is about 10%.
Diagnosis: Besnoitiosis can be diagnosed by biopsy examination of affected skin or other areas. The spherical, encapsulated cysts are pathognomonic. There may be a severe granulomatous reaction in young cysts or those which have broken and released their trophozoites, but there is usually little reaction except for the formation of the hyaline wall around the mature cysts.
Trophozoites are often found in blood smears, sometimes in large numbers, but most of them are introduced when a cyst is cut in obtaining blood.
Treatment: None known.
Prevention and Control: Until the mode of transmission is learned, the appropriate preventive measures must remain unknown. However, sanitary measures would prevent the spread of besnoitiosis if transmission is by ingestion, and insect control would prevent it if transmission is by biting insects, as some believe.