Quantitative determination of coccidian oocysts in beef calves from the coastal plain area of Georgia (U.S.A.).

For two consecutive years, determinations were made of the prevalence and abundance of coccidian oocysts from crossbred beef calves raised on Bahia grass pastures in the coastal plain area of Georgia. Of the 534 fecal samples collected during the survey, 461 (86.3%) contained one or more species of coccidian oocysts. The total mean oocysts per gram of feces (OPG) was significantly different (P less than 0.10) between the two years. Thirteen species of Eimeria were found during both years of the survey. Eimeria bovis was the most prevalent species found in the survey; E. ellipsoidalis, however, had the greatest number of OPG. Eimeria bukidnonensis, E. pellita, and E. brasiliensis were the least prevalent species and also had the lowest numbers of OPG. Only one clinical case of coccidiosis was seen. A nine-month-old calf had E. zuernii coccidiosis; it excreted E. zuernii oocysts in several fecal samples before the clinical disease appeared.

Physiologic basis of blood loss during Eimeria tenella infection.

Eimeria tenella-induced hemorrhage resulted in total blood losses of up to 10% of the body weight. Although packed cell volume was reduced 50%, neither plasma volume nor blood volume was significantly decreased, except briefly. The retention of lost blood in the ceca varied with the strain of E. tenella. Chicks infected with laboratory strain (L.S.) 24 passed most of the blood into the feces, whereas those infected with L.S. 49 retained most of the blood within the ceca.

Effects of Eimeria tenella infection and dietary aflatoxin on blood coagulation of young broiler chicks.

Eimeria tenella, aflatoxicosis, and a combination of the two prolonged the prothrombin times of male Cobb broilers. Factor V added to the plasmas of birds infected with E. tenella corrected the prothrombin time. E. tenella infection did not significantly alter the levels of plasma calcium, total plasma protein, or fibrinogen. Adding Factors V, VII, and X to plasma from birds with aflatoxicosis or aflatoxicosis plus E. tenella infection did not correct prothrombin times. Partial correction was achieved by adding normal plasma containing Factor II and fibrinogen. Plasma calcium and fibrinogen levels were not significantly altered in either group whereas total protein levels of these groups were significantly lower. The hemorrhage and mortality in birds infected with E. tenella may be explained in part by the longer prothrombin time resulting from deficiency of Factor V.

Decreased osmotic fragility of red blood cells of Eimeria adenoeides-infected turkeys.

The osmotic fragility of red blood cells (RBC) from Eimeria adenoeides-infected turkey poults was compared with that of RBC from control and water-deprived poults. At different hypotonic NaCl concentrations, lysis of RBC from infected poults was 10 to 35% less on day 4 postinoculation (PI) and 50 to 65% less on day 7 PI than that of controls. Red blood cells of poults deprived of water for 3 days were also resistant to lysis; the percent lysis was roughly the same as that of RBC from infected poults at day 7 PI. Incubating control RBC in plasma from infected poults, in extracts of infected ceca, or at different pH levels did not increase their resistance to lysis, suggesting that neither a stabilizing factor in the plasma that had rapid effect on the RBC nor a transient shift in blood pH was involved. Mean RBC size differed little among infected, water-deprived, and control poults (14.0-14.2 X 8.0-8.1 X 3.8 microns). However, although 3.5% of RBC population of control and water-deprived poults were immature (mid to late polychromatic erythrocytes), only 0.4% of the RBC of infected poults were immature. The data suggest that reduced water intake as well as other factors may be involved in the decreased osmotic fragility of RBC from poults infected with E. adenoeides.

Scanning electron microscopy of the cecal mucosa in Eimeria-tenella-infected and uninfected chickens.

Four major types of surface conformation were observed in the ceca of uninoculated control chickens. Spatulate villi were found in the cecal neck region, low ridges in the region where the neck expands, protruding collarlike structures in the mid cecal pouch, and flattened collars in the distal portion. In ceca infected with Eimeria tenella, there was some erosion and sloughing of the mucosal cells. These lesions were slight in the neck region, more severe in the dilated portion, most severe in the midregion, and moderate in the distal area. Oocysts were observed in the mucosal tissue of the cecal pouch.

Changes in moribund chickens as a result of Eimeria necatrix infection.

Chickens dying from Eimeria necatrix infection had clinical signs indicative of hypothermia, depleted carbohydrate stores, acidosis and kidney dysfunction. Blood lost into the intestine of infected chickens was great (15-22 ml). The body temperature of moribund chickens was 10 C lower than the control. Chickens dying from E. necatrix infection displayed similar physiological defects to those of chickens dying from E. tenella infection.

Comparison of the intestinal surface damage caused by Eimeria mivati, E. necatrix, E. maxima, E. brunetti, and E. acervulina by scanning electron microscopy.

Eimeria brunetti, an intestinal coccidial parasite of poultry, caused the most severe mucosal damage when compared to E. mivati, E. necatrix, and E. maxima. The damage caused by E. brunetti was observed in the ileum and large intestine and consisted of complete villar destruction in these areas. Oocysts of E. brunetti were observed in tissue debris. E. necatrix (jejunum) enlarged isolated villi causing the lamina propria core to extrude through the villus tip. Damage to the mucosal surface is not as severe as lesions observed on the serosal surface would indicate. E. maxima (jejunum) caused epithelial sloughing and isolated patches of exposed connective tissue. Oocysts of E. maxima were observed under the surface epithelial layer. E. mivati damaged the villus tips of the duodenum and caused sloughing of the villar epithelia exposuncated and clubbed the duodenal villi. E. mivati oocysts were observed in the infected epithelia.

Physiological basis of Eimeria tenella-induced mortality in individual chickens.

Chickens dying from Eimeria tenella infection revealed four major physiological stresses before death: (1) hypothermia, (2) depletion of carbohydrate stores, (3) metabolic acidosis, and (4) renal tubule-cell dysfunction. These stresses were less pronounced in chickens surviving the infection. Similar stresses could not be demonstrated in pair-feeding trials, in which uninfected chickens were fed only the amount consumed by infected chickens. Prolonged starvation of uninfected chickens only slightly altered the indicators used in assessing the stresses. The variability of previously reported plasma glucose values, in part, may be due to whether the birds tested were those on the verge of death or those that, ultimately, would survive the infection.

Effect of coccidiosis on blood coagulation in broilers.

Severe infection with Eimeria acervulina, Eimeria maxima, Eimeria necatrix, and Eimeria tenella increased the prothrombin times in broilers compared with the times in uninfected birds. Recalcification time was not affected. The increase in prothrombin time was related to the severity of infection (as measured by lesion score), and was significant (P less than or equal to 0.05) only in the most severely infected birds. The increase was of short duration, lasting only 1 or 2 days, and first appeared on day 5 or 6 postinoculation. Restricting the feed intake of uninoculated birds to the amount of feed consumed by infected birds showed that the reduction in feed intake with coccidiosis was not responsible for the increase in prothrombin time.

Changes in cecal composition with Eimeria tenella infection.

In each of three trials, the wet and dry weights of Eimeria tenella infected ceca were significantly increased compared to the control. The percentage of moisture and lipid in the cecal tissue remained unchanged or slightly increased. These effects were observed for all parasite strains examined and were detectable as early as day 4 postinoculation. Analysis of cecal protein and DNA suggested a uniform increase in cecal tissue rather than the production of a specific protein or component in response to the infection. Histological measurements of infected ceca, compared with the control, showed a twofold increase in both mucosal thickness and muscular thickness.

Effect of dietary aflatoxin on hemostasis of young turkey poults.

Young turkey poults fed graded levels of aflatoxin (0, 125, 250, and 500 microgram/kg) from hatching for 3 weeks displayed altered hemostasis, manifested in prolonged prothrombin times at 2 and 3 weeks of age. Body weights were only affected in those groups receiving 500 microgram/kg. Total plasma protein, fibrinogen, and plasma calcium were reduced in response to dietary aflatoxin. In comparison with chickens, which exhibit similar hemostatic dysfunction concomitant with reduced body weight, turkeys receiving aflatoxin at lower levels exhibited an altered hemostatic response without exhibiting depressed body weights. Thus, the turkey hemostatic system is a better indicator of aflatoxicosis than is body weight gain.

Relationship between Eimeria adenoeides infection and aflatoxicosis in turkey poults.

Three-week-old turkey poults receiving 250 micrograms/kg of dietary aflatoxin displayed prolonged prothrombin times due to decreased fibrinogen levels and depressed activity of factor II. Decreased body weights and increased mortality were also evident. Poults experiencing an Eimeria adenoeides infection had slightly increased prothrombin times that were not corrected by the addition of specific clotting factors. These birds exhibited significant reductions in total plasma protein levels. The combination of E. adenoeides and aflatoxicosis resulted in a significant depression in body weight, altered prothrombin time, and decreased levels of plasma calcium, protein, and fibrinogen. Increased mortality was also observed. E. adenoeides did not affect the hemostatic system of the turkey as severely as does aflatoxin. Turkeys were shown to be highly susceptible to aflatoxin when compared to chickens.

Eimeria tenella: cecal contraction in infected chickens.

The muscle of ceca from chickens infected with Eimeria tenella had an increased amplitude of contraction when compared to the cecal muscle of uninfected control chickens. The increased amplitude was significant (P less than or equal to 0.05) at 5 days postinoculation (PI) and became nonsignificant at 7 days PI. The amplitude also increased with the severity of the infection. The sensitivity of the muscle from infected ceca to acetylcholine (ACH) was greater than the control. Infection by different strains of E. tenella also increased the sensitivity of the cecal muscle to ACH when compared to the uninfected control. The rate of spontaneous contractions was not different in any group or treatment. The wet weight of infected ceca increased with days PI and severity of infection.

Surface changes induced by immune serum on Eimeria tenella sporozoites and merozoites.

The surface of merozoites and sporozoites of Eimeria tenella was affected by incubation with E. tenella-immune chicken serum (ICS). Normal chicken serum (NCS) and heat-inactivated ICS had no effect on the pellicular surface of either developmental stage. Sporozoites formed surface bulges or swellings after 10 min of incubation with ICS, and by 15 min postincubation, the morphology of the sporozoites was distorted by a surface coating of fibrinous material. Merozoites exposed to ICS were similarly coated, but surface swelling was not as severe. The coating formed rapidly and was seen as early as 5 min postincubation. Sporozoites incubated with heat-inactivated ICS supplemented with normal chicken serum were coated with a fibrinous material and in some cases lysed. These data indicated that complement must be present for the surface interaction to occur.