PubMed Health⌕ Search

Biomedical subjects

M E Cook

Publications and source records attributed to M E Cook.

100 records · Page 6Linked to original sources

Enhanced incidence of leg abnormalities in reovirus WVU 2937-infected chickens fed various dietary levels of selected vitamins.

Five experiments were conducted to evaluate the incidence of leg abnormalities of 4-, 6-, and 8-week-old reovirus WVU 2937-infected and uninfected chickens fed diets containing 20%, 100%, or 200% of the 1977 National Research Council nutrient requirements (NRC-77) of poultry for manganese, biotin, niacin, choline, or folic acid. Reovirus infection significantly elevated the incidence of leg abnormalities in the biotin-, niacin-, and folic-acid-deficient chickens and decreased the incidence of leg abnormalities in choline-deficient chickens. Reovirus-infected male chickens had a significantly greater incidence of leg abnormalities than reovirus-infected female chickens in the biotin, niacin, and folic acid studies. No sex differences in the incidence of leg abnormalities were observed in uninfected chickens. The incidence of leg abnormalities decreased with increasing dietary levels of biotin, niacin, choline, or folic acid in all chickens except reovirus-infected male chickens in the biotin study. In the manganese study, neither reovirus infection nor dietary level had any effect on the incidence of leg abnormalities in male or female chickens.

Age Factors↗

Severity of tenosynovitis in reovirus-infected chickens fed various dietary levels of choline, folic acid, manganese, biotin, or niacin.

Five experiments were conducted to determine the incidence and severity of tenosynovitis in tendons distal to the tarsal joint in 4-, 6-, and 8-week-old reovirus WVU 2937-infected chickens fed diets containing 20%, 100%, or 200% of the 1977 National Research Council nutrient requirements (NCR-77) of manganese, biotin, niacin, choline, or folic acid. Male chickens, but not female chickens, fed 20% or 100% or the NRC-77 level of folic acid had consistently higher lesion scores of tenosynovitis than male chickens fed the 200% NRC-77 level of folic acid. Increasing dietary manganese levels from 20% to 200% NRC-77 reduced the severity of tendon swelling in 6- and 8-week-old male chickens and appeared to increase the severity of tendon swelling in 8-week-old female chickens. Male chickens fed 20% of the NRC-77 required level of biotin had numerically more severe tenosynovitis at 6 weeks of age and significantly more severe tenosynovitis at 8 weeks of age than male chickens fed 100% and 200% of the NRC-77 level of biotin. Increasing dietary choline levels from 20% to 200% of the NCR-77 required level increased the severity of tenosynovitis numerically at 6 weeks of age and significantly at 8 weeks of age. When data were pooled across diet, male chickens had significantly more severe tenosynovitis than female chickens at 4, 6, and 8 weeks of age in the choline experiment and at 4 and 6 weeks of age in the folic acid experiment. Differences in the severity of tenosynovitis of individual treatment means (sex X diet X infection interaction means) occurred at only the 20% or 100% NRC-77 level of choline or folic acid. Male chickens also had more severe tenosynovitis than female chickens when fed 20% of the NRC-77 required level of manganese for 6 or 8 weeks.

Age Factors↗

Effect of reovirus infection and dietary levels of selected vitamins on immunocompetence of chickens.

The immunocompetence of 8-week-old reovirus WVU 2937-infected and uninfected chickens fed various dietary levels of biotin, niacin, choline, or folic acid was evaluated in four experiments. Antibody production to sheep red blood cells (SRBC), wattle responses to phytohemagglutinin-P (PHA-P), and wattle responses of tuberculin-sensitized chickens to bovine-purified protein derivative (PPD) were examined in five chickens per treatment. Dietary deficiencies had no effect on the in vivo T-cell immune responses to PPD, PHA-P, or humoral hemagglutinating-antibody production to SRBC. Reovirus-infected and uninfected chickens fed biotin at double the National Research Council (1977) requirement demonstrated decreased PPD responses. Lower hemagglutinating-antibody titers in the uninfected chickens and increased titers in the infected chickens were observed in those fed 200% of the requirement of biotin when compared with the chickens fed 20% and 100% biotin diets. Reovirus infection had no effect on PPD and PHA-P responses. However, in the choline experiment, reovirus-infected chickens had elevated titers. These data indicate that reovirus infection had no adverse effect on the immunocompetence of chickens 8 weeks postinfection. Dietary deficiencies also had no adverse effect on the immunocompetence of 8-week-old reovirus-infected and uninfected chickens.

Animals↗

Zinc deficiency in pheasant chicks fed practical diets.

A disease syndrome characterized by abnormal feathering and varus deviation of the tarsometatarsus spontaneously occurred in pheasant chicks fed a practical commercially prepared diet. The addition of supplemental Zn to the commercial diet was effective in alleviating the clinical signs, even though the commercial mix had Zn levels that met the published pheasant chick requirement. Supplemental arginine was ineffective in reducing the severity of the clinical signs. Also, when the diet was mixed in a laboratory setting, pheasant chicks did not develop abnormal feathering and leg bones. Clinical signs caused by feeding the commercial mix were not reproduced by altering dietary calcium and phosphorus levels in the laboratory mix. Neither adding a pellet binder nor removing supplemental Zn from the lab mix produced as severe leg and feather deformities as the commercial mix. Thus, unidentified dietary factors are capable of causing a Zn-deficiency syndrome in pheasant chicks fed practical diets with analyzed Zn levels meeting the required levels.

Animal Feed↗

Induction of tibial dyschondroplasia and suppression of cell-mediated immunity in chickens by Fusarium oxysporum grown on sterile corn.

An isolate of Fusarium oxysporum from corn associated with Kaschin-Beck disease in humans was tested for its ability to induce tibial dyschondroplasia (TD) and toxicity in chicks. Both leghorn and broiler chicks were fed diets in which corn was replaced with varied amounts (0% to 50%) of the F. oxysporum culture grown on sterile corn, or with known TD-inducing agents. F. oxysporum did not affect body weight in either type of chicks. In leghorn chicks, neither F. oxysporum nor the known TD-inducing agents (F. equiseti, 4%; tetramethylthiuram disulfide [Thiram], 35 ppm) caused TD. However, F. oxysporum at high levels (50%) and the two known TD-inducing agents reduced interdigital cutaneous response to phytohemagglutinin-P challenge. In addition, Thiram also reduced body-weight gain by more than 17%. In female broiler chicks (Cornish Rock), F. oxysporum not only decreased cell-mediated cutaneous response to phytohemagglutinin-P but also increased TD incidence; these same effects were observed with F. equiseti and Thiram. Histological examinations revealed similar pathological changes among dyschondroplastic lesions induced by F. oxysporum, F. equiseti, and Thiram. Results of this experiment indicate that the isolate of F. oxysporum from the region in which Kaschin-Beck disease is endemic can induce TD in broiler chicks and that it is immunosuppressive.

Animal Feed↗

Salt toxicosis in commercial turkeys.

Salt toxicosis was confirmed in a flock of 20,000 thirteen-week-old tom turkeys experiencing an increase in mortality. Clinical signs included polydipsia, diarrhea, ataxia, incoordination, tremors that progressed to depression, sternal and lateral recumbency accompanied by torticollis, and death. Mortality over a 5-day period was 6.7%. Necropsy lesions included pallor and dehydration of pectoral muscles, hepatic congestion, and fluid-filled small and large intestines. Microscopic lesions consisted of bilaterally symmetrical areas of necrosis within the cerebral hemispheres accompanied by vascular congestion and edema, as well as hyalinization of the glomerular capillary walls of the kidney and eosinophilic granular casts in the renal tubules. Average salt concentration in the feed from affected houses with 8.04%.

Animals↗

Histological study of tibial dyschondroplasia-like lesion from light-type chicks fed cysteine-supplemented diets.

Tibial dyschondroplasia (TD)-like lesions were induced in New Hampshire x Single-Comb White Leghorn cross chicks (NH x SCWL) by feeding excess levels of cysteine. The chicks fed a corn/soybean-meal-based diet had no spontaneous TD. The chicks fed the basal diet supplemented with 1.5% or 3.0% cysteine showed more than 50% TD-like lesions at 10 days of age; in another experiment, 1.6% cysteine induced TD (15%) at 3 weeks of age. A low incidence of rachitic-like lesions was found in Expt. 2 but was not associated with the dietary treatments. The TD-like lesion had a normal upper growth plate and a large mass of cartilage extending into the metaphysis; in contrast, the rachitic-like lesion had a widened upper growth plate. Microscopic examinations of the growth plates showed a widened prehypertrophic zone for the TD-like lesion and a widened proliferative zone for the rachitic-like lesion compared with the normal growth plate.

Animals↗

Non-reducible collagen cross-linking in cartilage from broiler chickens with tibial dyschondroplasia.

Recent work has shown that hydroxylysylpyridinoline (HP), a non-reducible cross-link that stabilizes the collagen fibril network, is significantly greater (over 10-fold) in dyschondroplastic cartilage than in normal growth-plate cartilage in the tibiotarsi of chickens with homocysteine-induced tibial dyschondroplasia (TD). In the present study, broiler chicks with a genetic disposition to TD, as well as normal broiler chicks on a copper-deficient diet alone or supplemented with copper and thiram, were raised for 3 to 4 weeks (Expts. 1 and 2). Their dyschondroplastic cartilage from the proximal tibiotarsus was collected and analyzed for HP as well as lysylpyridinoline (LP) cross-links. Normal growth plate cartilage was obtained from chicks on the copper-deficient diet supplemented with copper. In a third experiment, another set of broiler chicks was raised on a corn/soybean meal-based diet with or without homocysteine, and their articular and sternal cartilage were isolated for cross-link analysis. In the first two experiments, dyschondroplastic cartilage from all birds with induced TD had higher HP and LP concentrations than growth-plate cartilage from birds without TD, although the ratios of HP to LP varied. In the third experiment, the sternal and articular cartilage from birds with homocysteine-induced TD appeared normal, having similar HP concentrations in the same types of cartilage in birds without TD.

Amino Acids↗

Tibial dyschondroplasia of chickens induced by Fusarochromanone, a mycotoxin.

Chicks were fed for 3 weeks a practical broiler starter diet amended with fusarochromanone (FC), a mycotoxin. In Hubbard broiler chicks, the highest test dose of FC (75 ppm) suppressed body weight by 33% and humoral response to sheep erythrocytes by 34% to 50%, and increased the incidence of tibial dyschondroplasia (TD) to 100%. The intermediate dose (35 ppm) significantly increased the incidence of TD in both types of broiler chicks (Hubbard and Indian River), but its effect on humoral response to sheep erythrocytes was not consistent across several experiments. A minimum dietary concentration greater than 20 ppm was required to significantly increase the incidence of TD. Excessive dietary copper or zinc (200 ppm) alleviated the effect of FC on TD. However, activities of copper-dependent ceruloplasmin and superoxide dismutase was not affected by FC. Cartilage mineral profiles in FC- or Thiram-induced TD differed from that of 1-day-old hypertrophic embryonic cartilage core (less K and Mn). FC did not induce TD in leghorn chicks.

Amino Acids↗

Elevated plasma glycosaminoglycans in chickens with tibial dyschondroplasia induced by a Fusarium oxysporum isolate.

Chicken plasma glycosaminoglycans (GAGs) were isolated and digested. Their building block molecules, namely, glucosamine and galactosamine, were quantified by gas chromatography. The levels of these two amino sugars were elevated in broiler chickens with tibial dyschondroplasia (TD) induced by culture material of Fusarium oxysporum (FO), a mold isolated from corn originated from the endemic region of Kaschin-Beck disease (KBD) in China. As the TD severity score changed from 1 (healthy) to 2, 3, and 4, glucosamine increased by 10%, 33%, and 57% and galactosamine by 9%, 13% and 48%, respectively. The elevated plasma GAGs correlated to TD severity but not to the amount of FO material in the diets. This correlation of plasma GAGs to TD in chickens parallels the reported correlation of urinary GAGs to KBD in humans. The possibility of TD as an animal model for KBD is discussed.

Animals↗