Coccidial infections and gut microflora.

Oral inoculations of sporulated oocysts of Eimeria acervulina, E. necatrix, E. brunetti, E. tenella, or none were given to five groups of 4-wk-old chicks. Fecal samples were taken at 1, 3, 5, 6, 7, 8, 11, 14, and 21 days postinoculation and total fecal aerobe, total fecal anaerobe, fecal lactobacilli, and fecal coliform concentrations were enumerated. Fecal aerobe concentrations increased 10-fold during the period from 3 to 8 days postinoculation. Fecal anaerobe concentrations had small increases from 3 to 6 days. Fecal lactobacilli concentrations increased with E. necatrix and E. brunetti infections but decreased with E. tenella infections. Fecal coliform concentrations increased most with the duodenal infections and increased less with posterior tract infections.

Microelements in the circulation of coccidiosis-infected chicks.

Four-week-old Single Comb White Leghorn male chicks were inoculated with either Eimeria acervulina, E. necatrix, E. brunetti, E. tenella, or left uninfected. On Days 1, 3, 5, 6, 7, 8, 9, 10, 14, 21, 28, and 35 after inoculation, blood was removed from five birds in each group; content of copper, zinc, and iron in plasma and total iron-binding capacity were determined. Copper content in plasma was increased during the acute phase of the infections by lower intestinal tract (E. brunetti, E. tenella) infections but not by upper tract (E. acervulina, E. necatrix) infections. Zinc content in plasma was decreased by E. acervulina and E. necatrix infections on the 7th day and was increased by E. acervulina, E. brunetti, and E. tenella infections on the 9th or 10th days. Iron content in plasma was decreased during the acute phase (Days 5 to 7) of E. acervulina, E. brunetti, and E. tenella infections. Total iron-binding capacity was decreased by acute phase E. acervulina and E. brunetti infections. Eimeria tenella infections increased total iron-binding capacity during both the acute and early recovery phases. Plasma content of all components returned to normal by the latter part of the recovery phase of the infections and remained so thereafter. Plasma trace mineral content appeared to be influenced by mineral absorption effects, by hemorrhaging, and perhaps by invasion of the bloodstream by gut bacteria as a result of mucosal damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Macroelements in the circulation of coccidiosis-infected chicks.

Four-week-old Single Comb White Leghorn (SCWL) chicks were inoculated with either Eimeria acervulina, E. necatrix, E. brunetti, E. tenella, or left uninfected. On the 1st, 3rd, 5th, 6th, 7th, 8th, 9th, 10th, 14th, 21st, 28th, and 35th days after inoculation, blood was removed from five birds in each group, and the content of calcium, magnesium, sodium, potassium, hemoglobin, erythrocytes, and packed cell volumes were determined. Hemoglobin, erythrocyte concentrations, and hematocrits all decreased during the acute phase of the infections and returned to normal during recovery. Plasma calcium concentrations were significantly decreased by the upper intestinal tract infections, but decreases were smaller in lower tract infections. Plasma magnesium was decreased and then increased by lower tract infections, but upper tract infections had variable effects. In contrast to earlier reports, acute phase E. acervulina, E. brunetti, and E. tenella infections decreased sodium plasma concentrations. Plasma potassium concentrations were variable, but increases were associated with the induction phases of E. necatrix and E. brunetti infections.

Coccidial infections and manganese absorption.

Four-week-old Single Comb White Leghorn male chicks were infected with 1,000,000 sporulated oocysts of Eimeria acervulina, or with 50,000 sporulated oocysts of E. necatrix, or with 50,000 sporulated oocysts of E. brunetti, or with 50,000 sporulated oocysts of E. tenella, or were left uninfected as the controls. On Days 1, 3, 6, 10, 14, 21, and 28 following the infection, 5 birds from each group were randomly selected and administered 2.0 microCi of 54Mn orally. At 1, 2, and 4 hr after administration of the radiotracer, the amount of radioactivity appearing in the bloodstream was measured. The absorption of manganese 6 days after the beginning of the E. acervulina infections was decreased to 23 to 34% of that in the uninfected birds, whereas E. necatrix infections resulted in a smaller and more variable decrease in manganese absorption. The other coccidial infections did not decrease manganese absorption significantly. On the 14th day of the infections, all four coccidial infections increased manganese absorption two- to fourfold that found in the controls in one trial but not in the second trial. At other times during the coccidial cycle, no effects were seen on manganese absorption.

The anatomy of the avian digestive tract as related to feed utilization.

The anatomy of the avian GI tract is believed to markedly influence the utilization of feed processed by it. The anterior portion of the tract is adapted for ingestion, storage, and partial digestion of starch and proteins. The structure of the avian intestine is similar to that of other monogastrics except that lacteals are not found. Damage to the intestinal epithelium may decrease nutrient absorption, whereas epithelial replacement may result in improved nutrient utilization. Mitochondrial and other organelle changes are associated with changes in nutrient absorption. The avian intestine has a prominent glycocalyx overlying the microvilli. The avian liver lacks the true lobular structure of the mammalian liver. The hepatocytes are arranged in plates two cell layers thick around the bile caniculi. The avian pancreatic structure contains two main and two smaller lobes containing acinar cells, which secrete digestive enzymes into the the pancreatic ducts, and endocrine cells, which secrete hormones into the general circulation. The structure of the colon is similar to that of the intestine except for poor enervation.

Coccidial infections and iron absorption.

Four-week-old chicks were infected with single oral doses of 1,000,000 sporulated oocysts of Eimeria acervulina, or 40,000 sporulated oocysts of E. necatrix, or 50,000 sporulated oocysts of E. brunetti, or 50,000 sporulated oocysts of E. tenella, or left uninfected. At intervals of 1, 3, 6, 10, 14, 21, 28, and 35 days after infection, absorption of 5 muCi Fe-59 was measured in five birds selected at random from each of the five experimental groups. Iron absorption was markedly decreased during the acute phase (day 6) of E. acervulina infections, less marked decreases were observed in E. necatrix infections, while no decreases in iron absorption were seen in the acute phase (day 6) of E. brunetti and E. tenella infections. Thus, the most critical area of the intestine for iron absorption, as shown by the largest decrease in amount of iron absorbed during the acute phase of coccidial infections, was located in the duodenum. During the recovery phase of all infections, periods of increased iron absorption were seen. This effect was marked in E. acervulina and E. tenella infections.

Effect of Eimeria species on the appearance of radioactivity in the blood of chicks fed radio-labeled glucose or 3-0-methyl-D-glucose.

Results of five trials with four species of coccidia (Eimeria acervulina, E. necatrix, E. tenella, and E. brunetti) failed to demonstrate any interference with glucose absorption in the parasitized intestines of intact chick hosts. In addition, circulating blood radioactivity in severely parasitized chicks, as evidenced by weight gain data and intestinal lesion scores, was significantly higher than that in control chicks following oral administration of 14C-glucose or 3-0-methyl-D-14C-glucose at 6 days postinfection. During the recovery phase of the infection (14 to 21 days postinfection), severely infected chicks rapidly gained weight and the blood radioactivity of parasitized chicks was consistently higher than that of uninfected control chicks. No significant differences in weight or blood radioactivity were observed during the post-recovery period (28 to 35 days postinfection).

Effect of zinc deficiency on the ultrastructure of the pancreatic acinar cell and intestinal epithelium in the rat.

Ultrastructural changes in the pancreatic acinar cell and intestinal epithelium were studied in rats fed a zinc-deficient diet as compared with those of pair-fed and ad libitum fed zinc-supplemented controls. The pancreatic acinar cells of zinc-deficient rats showed marked cellular alterations: a reduction in zymogen granules, rupture of zymogen granules, basal accumulation lipid droplets, prominent lysosome-like bodies, focal degradation of the cytoplasm, and intracistenal granules within the dilated cisternae of the endoplasmic reticulum. The Golgi complex appeared inactive, and nuclear pyknosis was noted. Defects in the endoplasmic reticulum and ribosomes were shown by their presence in the foci of cytoplasmic degradation, which were subsequently subject to lysosomal digestion and degeneration. The microvilli of the intestinal epithelium in the zinc deficient rats were well organized and normal in size, demonstrating a typical geometric array when cross-sectioned. The intercellular boundaries, the junctional complexes, and the terminal web were well developed and appeared intact. However, the cell cytoplasm showed prominent cellular changes: an abundance of lysosome-like bodies, membrane-bound autopraphic vacuoles, sparse endoplasmic reticulum, a quiescent-appearing Golgi complex with tightly packed lamellae containing few vacuoles, pyknotic nuclei, and a dilated nuclear periphery.

Effect of zinc deficiency on intestinal transport triglyceride in the rat.

Ultrastructural and biochemical changes in the intestinal epithelium during the process of active triglyceride absorption were studied in rats fed a zinc-deficient diet as compared with those of pair-fed and ad libitum-fed zinc-supplemented controls. The rate of triglyceride absorption markedly decreased in zinc-deficient rats. Despite a significant reduction in pancreatic lipase activity, the digestion of triglycerides proceeded normally in the zinc deficient rats, as evidenced by no apparent signs of diarrhea (or steatorrhea) and by the appearance of the hydrolytic products such as free-fatty acids and monoglycerides in the intestinal mucosa. The mucosa uptake of digested lipids and resynthesis of triglycerides in the mucosa from deficient rats were normal. Ultrastructural and chromatographic analysis of the mucosal lipids indicated a massive accumulation of lipid droplets, predominantly in the form of triglycerides. The primary defect in lipid absorptive processes in zinc-deficient rats occurred in the formation of chylomicrons. The lipid droplets in the mucosa of deficient rats were physically unstable. This instability was shown by coalescence of droplets which did not appear to be membrane-bound. Coalescing lipid droplets ranged from 2.0 to 4.0 micron in diameter. The absorptive cells were not able to discharge lipid droplets of this size into the intercellular spaces and hence into the lamina propria, resulting in the accumulation of the large droplets within the mucosa. This exit block to the movement of lipid droplets out of the mucosal cell appeared to be due to the failure, in zinc-deficiency, of the mucosal synthesis of proteins required for the formation of chylomicrons. Ultrastructural observations demonstrated changes in the subcellular organelles related to protein synthesis, including a marked reduction in granular endoplasmic reticulum and a quiescent appearance of the Golgi-complex.

Ingested polychlorinated biphenyl Aroclor 1242 and growth, calcium and zinic absorption, and intestinal ultrastructure in chicks.

Decreased growth, edema, labored breathing, internal hemorrhaging, and high mortality were seen in chicks fed 48 or 197 p.p.m. Aroclor 1242 for 7 weeks. Calcium absorption was increased when birds were fed 197 p.p.m. PCB while zinic absorption was increased in birds fed both levels of PCB. Duodenal mucosal cell respiration rates were unaffected by either PCB treatment. Upon ultrastructural examination, mitochondrial alterations, lipid accumulations in the lamina propriae, edema, and swollen endoplasmic reticula were found in duodenal mucosal cells. Necrotic areas were found in the kidney proximal tubule region of PCB fed birds.