Eimeria Necatrix

Host: Chicken.

Location: The first and second generation schizonts are found in the small intestine and the third generation schizonts, gametes and gametocytes in the ceca.

Geographic Distribution: Worldwide.

Prevalence: Common.

Morphology: The oocysts are oblong ovoid, 12 to 29 by 11 to 24 u with a mean of 20 by 17 u (Becker et al., 1956). The oocyst wall is smooth and colorless, without a micropyle. An oocyst polar granule is present. An oocyst residuum is absent. The sporocysts are elongate ovoid, with a Stieda body. A sporocyst residuum is absent. The sporulation time is 2 days (18 hours at 29 C according to Edgar, 1955).

Life Cycle: Chickens become infected by ingesting sporulated oocysts. When the sporozoites emerge, Van Doorninck and Becker (1957) found that they first enter the epithelial cells of the villi in the small intestine, pass thru the epithelium into the lamina propria or core of the villus and migrate toward the muscularis mucosae. Most of them are engulfed by macrophages en route and are transported by them to the epithelial cells of the fundus. The macrophages invade these cells and appear to disintegrate during or after the invasion process, leaving the sporozoites unharmed. These then round up to form first generation schizonts.

The remainder of the life cycle has been studied by Johnson (1930) and Tyzzer, Theiler and Jones (1932). Both the first and second generation schizonts are found above the host cell nuclei in the epithelial cells of the gland fundi. The first generation merozoites are liberated 2.5 to 3 days after infection and enter adjacent epithelial cells. The second generation schizonts are relatively large, measuring 39 to 66 by 33 to 54 u with a mean of 52 by 38 u. Most of the second generation merozoites are liberated 5 to 7 days after infection, but a few may still be liberated as long as 23 days after infection. They measure 8 to 11 by 1.5 to 2.0 u with a mean of 9 by 2 u. They pass to the cecum, where they penetrate the epithelial cells, coming to lie below the host cell nuclei, and turn into third generation schizonts. Most of them are found in the surface epithelium, but some enter the glandular epithelium. Multiple infections of a cell with 3 or 4 schizonts may occur. These third generation schizonts are relatively small and contain only 6 to 8 or a maximum of 16 third generation merozoites. It is not certain whether there is more than one asexual generation in the cecum.

The third generation and some of the second generation merozoites enter other cecal epithelial cells and become macrogametes or microgametocytes. These also lie below the host cell nuclei. Microgametes develop from the microgametocytes, fertilization takes place, and oocysts form and are released. The prepatent period is 7 days, and the patent period is about 12 days.

Brackett and Bliznick (1952a) reported that the number of oocysts produced by E. necatrix per oocyst fed ranged from 15 in a group of chicks infected with 35,000 oocysts each to 58,000 in another group in which the infective dose was 50 oocysts.

Pathogenesis: Next to E. tenella, this is the most pathogenic and important species of chicken coccidium. Indeed, with the decrease in importance of E. tenella due to the use of coccidiostatic drugs, E. necatrix has come to the fore in many areas as the cause of more losses than E. tenella.

E. necatrix is often said to cause a more chronic type of coccidiosis than E. tenella. This is not because it runs a longer course, but because it produces so much scar tissue in the small intestine that its effects are more lasting.

The pathogenesis of E. necatrix has been studied especially by Tyzzer, Theiler and Jones (1932). The principal lesions are in the small intestine, the middle third of which is most seriously affected. Small, white, opaque foci are found here by the fourth day after infection. They are composed of second generation schizonts developing deep in the mucosa. They are so deep that they can be seen thru the serosa but not from the mucosal surface of the intestine. They are seldom more than a millimeter in diameter, but may coalesce and thus appear larger. Severe hemorrhage may appear on the 5th or 6th days. The small intestine may be markedly swollen and filled with clotted or unclotted blood. Its wall is greatly thickened, dull red, and many petechial hemorrhages appear in the white, opaque foci which by now contain second generation merozoites. The gut wall may lose contractility, become friable and even appear gangrenous. The epithelium may slough, and by the end of the 6th day a network of fibrin containing mononuclear cells appears in the destroyed areas. This is later replaced by connective tissue, and permanent scarring results which interferes with intestinal absorption.

There is less anemia than in E. tenella infections. Using the microhematocrit technic, Joyner and Davies (1960) found that the packed red cell volume decreased from 28% to 23% seven days after experimental infection with 20,000 oocysts, and to 25% after infection with 10,000 oocysts, but that there was no significant decrease after infection with 1000 oocysts. The hematocrit levels had not returned to the original level 12 days after infection.

The ceca are not seriously affected. They may be contracted and their contents may be dehydrated.

Death usually occurs 5 to 7 days after infection. Many of the birds which recover remain unthrifty and emaciated. The after-effects of this type of coccidiosis are often so long-lasting that it is not worthwhile to keep birds which have recovered from severe attacks.

Brackett and Bliznick (1950, 1952) found that inoculation with 25,000 to 50,000 oocysts (a relatively small number) caused a high degree of mortality in young chickens. Following inoculation with equal numbers of oocysts, young birds are more severely affected than older ones, but if the inocula are calculated on a weight basis, older birds may be more severely affected than younger ones. In 3-week-old chicks, 25,000 oocysts caused a mortality of 87%, while in 4-week-old chicks, 18,000, 37,000, 75,000 and 150,000 oocysts caused mortalities of 8, 75, 85 and 61%, respectively.