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The aim of this study was to determine the binding capacity of a hydrated sodium calcium aluminosilicate (HSCAS) for aflatoxin B(1) (AFB(1)), and the efficacy of the HSCAS to reduce the concentrations of residual AFB(1) and its metabolites in the liver and kidney of broilers fed AFB(1). One hundred 1-d-old male broilers (Ross 708) were maintained in chick batteries and allowed ad libitum access to feed and water. A completely randomized design was used with 5 replicate pens of 5 chicks assigned to each of 4 dietary treatments from hatch to 21 d. Dietary treatments included the following: A) basal diet (BD), with no HSCAS or AFB(1), B) BD supplemented with 0.5% HSCAS only, C) BD supplemented with 2.5 mg of AFB(1)/kg of feed, and D) BD supplemented with 2.5 mg of AFB(1)/kg of feed and 0.5% HSCAS. On d 21, 5 chicks from each treatment were anesthetized with carbon dioxide, killed by cervical dislocation, and samples of liver and kidney were collected for analysis of AFB(1) residues. The percentage of AFB(1) bound for each concentration of adsorbent (100, 10, 1, 0.5, 0.25, and 0.05 mg/10 mL) was 100, 91.1, 81.8, 75.4, 40.1, and 8.8%, respectively. Concentrations of aflatoxin residues (AFB(1), aflatoxicol, aflatoxins B(2) and G(1)) were lower (P < 0.05) in livers and kidneys of birds fed AFB(1) plus HSCAS (diet D), when compared with birds fed AFB(1) alone (diet C). However, histopathology data from the in vivo study indicated that HSCAS did not prevent lesions associated with aflatoxicosis. The decrease in the bioavailability of AFB(1) caused by the HSCAS reduced aflatoxin residues in liver and kidney, but not enough to completely prevent the toxic effects of AFB(1) in broilers.

A study was conducted to determine the toxicity of melamine in young broilers fed graded levels of melamine. An additional objective was to determine melamine residual levels in selected tissues. One hundred and seventy-five 1-d-old male Ross broiler chicks were sorted to a randomized block design in stainless steel battery pens. Chicks were assigned to 7 dietary treatments containing 0, 0.5, 1.0, 1.5, 2.0, 2.5, and 3.0% melamine. Each dietary treatment was fed to 5 replicate pens of 5 chicks for 21 d. Mortality increased quadratically (P<0.001) with increasing dietary concentrations of melamine. However, compared with controls, mortality was only higher (P<0.001) in birds fed≥2.5% melamine. Feed intake decreased linearly (P<0.001), whereas BW gain decreased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, both feed intake and BW gain were lower (P<0.001) only in birds fed≥1.0% melamine. Relative kidney weights increased linearly (P<0.001), whereas relative liver weights increased quadratically (P<0.05) with increasing dietary concentrations of melamine. Melamine residues in breast muscle and liver tissue increased linearly (P<0.001) with increasing dietary concentrations of melamine, whereas melamine residues in kidney and bile increased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, melamine concentrations in liver and kidney were higher (P<0.001) in birds fed all levels of melamine, whereas melamine concentrations in breast muscle and bile were only higher (P<0.001) in birds fed≥1.0% melamine. Serum albumin, total protein, globulin, and calcium increased quadratically (P<0.02) in birds as dietary melamine increased, whereas serum aspartate transaminase and gamma gluatamyltransferase increased linearly (P<0.01) with increasing levels of melamine in the diet. Renal histopathology revealed nonpolarizable melamine crystals in the collecting tubules and ducts of birds fed≥1.5% melamine. In summary, dietary melamine was toxic to broilers at concentrations≥1.0%.

A 3-wk feeding study was conducted to evaluate the efficacy of turmeric (Curcuma longa) powder (TMP), containing a known level of curcumin, and a hydrated sodium calcium aluminosilicate (HSCAS; Improved Milbond-TX, IMTX, an adsorbent, Milwhite Inc., Houston, TX) to ameliorate the adverse effects of aflatoxin B(1) (AFB(1)) in broiler chicks. Four pen replicates of 5 chicks each were assigned to each of 7 dietary treatments, which included the basal diet not containing TMP, HSCAS, or AFB(1) (control); basal diet supplemented with 0.5% food grade TMP that contained 1.48% total curcuminoids (74 mg/kg); basal diet supplemented with 0.5% HSCAS; basal diet supplemented with 1.0 mg/kg AFB(1); basal diet supplemented with 0.5% TMP and 1.0 mg/kg AFB(1); basal diet supplemented with 0.5% HSCAS and 1.0 mg/kgAFB(1); and basal diet supplemented with 0.5% TMP, 0.5% HSCAS, and 1.0 mg/kg AFB(1). The addition of TMP to the AFB(1) diet significantly (P < 0.05) improved the weight gain of chicks, and the addition of HSCAS to the AFB(1) diet significantly (P < 0.05) improved feed intake and weight gain, and reduced relative liver weight. The addition of TMP or HSCAS and TMP with HSCAS ameliorated the adverse effects of AFB(1) on some of the serum chemistry parameters (total protein, albumin, cholesterol, calcium). Further, decreased antioxidant functions in terms of level of peroxides, superoxide dismutase activity, and total antioxidant concentration in liver homogenate due to AFB1 were also alleviated by the inclusion of TMP, HSCAS, or both. The reduction in the severity of hepatic microscopic lesions due to supplementation of the AFB(1) diet with TMP and HSCAS demonstrated the protective action of the antioxidant and adsorbent used in the present study.

Three hundred 1-day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups of 150 each. One group was maintained on quail mash alone, whereas Fusarium verticillioides culture material (FCM) was added to quail mash in the second group from 5 days of age and supplied 150 mg FB1/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units [cfu]/ml) was given to groups CS and FS at 21 days of age. Three quail each, were necropsied on day 21 (0 day interval) from groups CX and FX, whereas at subsequent intervals, i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection (DPI), they were sacrificed from all four groups (CX, CS, FX, and FS) to study the agglutinin response to Salmonella Gallinarum and pathologic changes. The agglutinin titers to Salmonella Gallinarum in the combination group (FS) were generally lower when compared with those in group CS. A reduction in the size of spleen along with depletion of white pulp, thinning of cardiomyocytes, lymphoid cell depletion from bursal follicles, and renal tubular nephrosis were characteristic pathologic changes in group FX. In contrast, there was mild to severe enlargement of spleen accompanied by necrosis and reticuloendothelial cell hyperplasia, pericarditis, myocarditis, and focal interstitial nephritis in groups CS. Similar but more severe lesions were observed in the combination group (FS). In addition, the flabby texture of heart, hydropericardium, and ascites were mainly observed in group FS. It is concluded that continuous presence of fumonisins at 150 mg/kg diet increases the severity of Salmonella Gallinarum infection in young Japanese quail.

Three hundred day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups with 150 quail in each group. One group was maintained on quail mash alone, while Fusarium moniliforme culture material was added to quail mash in the second group from day 5 of age and was supplied at a rate of 150 ppm fumonisin B1 (FB1)/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units/ml) was given to groups CS and FS at 21 days of age. Three quail each were necropsied on day 21 (0 day interval) from groups CX and FX only. At subsequent intervals (i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection [DPI]), three quail were euthanatized from all four groups (CX, CS, FX, and FS). The gross and microscopic lesions were recorded in both mortality and euthanatized birds at the above intervals. The ultrastructural studies were done at 5 DPI. Mild to moderate hepatomegaly and pale discoloration of liver were observed in group FX, while congestion, hemorrhages, necrosis, and mild to severe hepatomegaly were the predominant gross lesions in both infected groups (CS and FS). The gross lesions in quail inoculated with Salmonella Gallinarum alone (group CS) generally developed slowly, appeared more widely scattered, and involved comparatively less surface area in contrast to the rapidly progressive and frequently confluent lesions in the combination group (FS), especially in the first 5 days of infection. Mild to marked hepatocellular swelling, multifocal hepatic necrosis, and hepatocellular and bile duct hyperplasia were the characteristic microscopic changes in the FX group. Microscopic lesions in quail of group CS comprised congestion, vacuolar changes, and focal necrosis in early stages, followed by granulomatous lesions at later intervals. Similar but more severe lesions were observed in the combination group (FS). Based on transmission electron microscopy, the maximum effect of FB1 toxicity was observed on mitochondria and endoplasmic reticulum. In general, the mitochondriae showed diverse form and structure, some of which appeared to lose their intact outer membrane, and the mitochondrial cristae were disoriented. The deformity in the cisternae structure of rough endoplasmic reticulum, with their rearrangement into round or tubular forms either bearing granular surface or leading to accumulation of smooth endoplasmic reticulum, was evident only in groups FX and FS. We conclude that the continuous presence of fumonisins in the diets of young quail might increase their susceptibility to or the severity of Salmonella Gallinarum infection.

Information about the annual variation of trichomoniasis in mourning doves (Zenaida macroura) may be important in understanding mechanisms affecting mourning dove populations. The objectives of this study were to monitor the presence and annual variation of Trichomonas gallinae for 6 yr in a local mourning dove population using hunter-killed doves. During 1998-2003, 4052 hunter-killed doves were sampled for the presence of T. gallinae; 226 (5.6%) tested positive (4.4%-10.6% range). Results of the monitoring effort were relatively consistent during the 6-yr period, with the presence of T. gallinae being within the range of previously reported estimates for mourning doves. Asymptomatic carriers in one segment of the dove population may provide a mechanism for spreading the disease to other segments of the mourning dove population.

A 1520 bp region of Cochlosoma anatis mtDNA 16S gene was subjected to DNA sequencing and a 466 bp portion was compared with other protozoan 16S sequences to develop PCR primers specific for C. anatis. This PCR diagnostic method allowed identification of C. anatis from house flies, Musca domestica L., turkey gut, and fecal samples within 6 h after field-collected samples reached the laboratory. House flies detected carrying C. anatis using the diagnostic 374 bp amplicons represented the first record of this protozoan in house flies.

The individual and combined effects of feeding fumonisin B1 (FB1; 0, 100, 200 mg FB1/kg) and moniliformin (M; 0, 100, 200 mg M/kg) were evaluated using a 3 x 3 factorial arrangement of treatments. Significant mortality (P < 0.05) occurred in chicks fed all diets containing 200 mg M/kg (50%-65%). Compared with controls and chicks fed FB1, both feed intake and body weight gain were decreased (P < 0.05) in chicks fed diets containing 100 mg M/kg. Chicks fed M had heavier heart weights (P < 0.05) than control chicks or chicks fed FB1. Compared with controls, chicks fed diets containing 200 mg M/kg or a combination of 200 mg FB1/kg and 100 mg M/kg had increased kidney and liver weights (P < 0.05). Significant FB1 by M interactions (P < 0.05) were observed for serum total protein and aspartate aminotransferase. Mild to moderate periportal extramedullary hematopoiesis and mild focal hepatic necrosis were observed in chicks fed FB1 alone. An increased incidence of large pleomorphic cardiomyocyte nuclei, loss of cardiomyocytes, and mild focal renal tubular mineralization were observed in chicks fed M alone. Both cardiac and renal lesions were observed in chicks fed combinations of FB1 and M. Data indicate FB1 and M, alone or in combination, can adversely affect chick performance and health at these dietary concentrations. The interactive effects of FB1 and M were not synergistic and were less than additive in nature. At the dietary concentrations studied, M is much more toxic to broilers than FB1.

Floor pen studies were conducted, with broilers from 1 to 7 wk of age and with turkeys from 1 to 14 wk of age, to evaluate the chronic effects of moniliformin (M). Fusarium fujikuroi (M-1214) culture material was added to typical corn-soybean basal diets to supply 0, 25, or 50 mg M/kg diet (broilers) or 0, 12.5, 25, 37.5, or 50 mg M/kg diet (turkeys). Compared with controls, chicks fed diets containing 50 mg M/kg consumed more feed, had lower body weight gain, were less efficient in converting feed to body weight gain, and had increased relative heart and proventriculus weights. Chicks fed the diet containing 50 mg M/kg also had significantly higher mortality and decreased mean corpuscular volumes compared with controls. Broilers fed 25 and 50 mg M/kg also had increased serum gamma glutamyltransferase activities. Feed intake, body weight gain, and feed conversion of turkeys fed dietary M were not affected. At 6 and 14 wk, turkeys fed 25, 37.5, or 50 mg M/kg diet had increased (P < 0.05) relative heart weights when compared with controls. At week 14, turkeys fed diets containing 37.5 or 50 mg M/kg also had increased (P < 0.05) relative liver weights compared with turkeys fed 0, 12.5, or 25 mg M/kg diet. Lesions, observed only in the hearts of broilers and turkeys fed 50 mg M/kg, were loss of cardiomyocyte cross striations, increased cardiomyocyte nuclear size, and an increased number of cardiomyocyte mitotic figures (turkeys only). Results indicate that > or = 37.5 mg M/kg is hepatoxic and > or = 25 mg M/kg is cardiotoxic to turkeys and 50 mg M/kg diet is toxic to broilers fed to market age.

Floor pen studies were conducted with 270 broiler chicks and 144 turkey poults, all 1 wk old, to evaluate the chronic effects of fumonisin B1 (FB1). A completely randomized design was used in both studies with six pen replicates of 15 chicks or eight pen replicates of six poults assigned to each of three dietary treatments from Weeks 1 to 7 (broilers) or to Week 14 (turkeys). Fusarium moniliforme (M-1325) culture material was added to a typical corn-soybean basal diet to supply 0, 25, or 50 mg FB1/kg diet. Feed intake, body weight gain, and feed conversion of chicks were not affected (P > 0.05) by FB1. Turkeys fed 50 mg FB1/kg had significantly (P < 0.05) lower feed intake than the controls. Compared with controls, chicks and turkeys fed FB1 diets had significantly higher liver sphinganine to sphingosine ratios (P < 0.05). Relative organ weights of chicks were not affected (P > 0.05) by FB1, other than those chicks fed 25 mg FB1/kg, which had lower (P < 0.05) relative proventriculus weights than the chicks fed 0 or 50 mg FB1/kg. Broilers fed 50 mg FB1/kg had decreased serum calcium and increased serum chloride when compared to broilers fed 0 or 25 mg FB1/kg. Hematology was not affected (P > 0.05) by dietary FB1. No lesions were present in any organ examined microscopically. Results indicate that 50 mg FB1/kg diet is detrimental to turkeys but is not toxic to broilers fed to market age.

Type A influenza viruses can infect a wide range of birds and mammals, but influenza in a particular species is usually considered to be species specific. However, infection of turkeys with swine H1N1 viruses has been documented on several occasions. This report documents the isolation of an H1N2 influenza virus from a turkey breeder flock with a sudden drop in egg production. Sequence analysis of the virus showed that it was a complex reassortant virus with a mix of swine-, human-, and avian-origin influenza genes. A swine influenza virus with a similar gene complement was recently reported from pigs in Indiana. Isolation and identification of the virus required the use of nonconventional diagnostic procedures. The virus was isolated in embryonated chicken eggs by the yolk sac route of inoculation rather than by the typical chorioallantoic sac route. Interpretation of hemagglutination-inhibition test results required the use of turkey rather than chicken red blood cells, and identification of the neuraminidase subtype required the use of alternative reference sera in the neuraminidase-inhibition test. This report provides additional evidence that influenza viruses can cross species and cause a disease outbreak, and diagnosticians must be aware that the variability of influenza viruses can complicate the isolation and characterization of new isolates.

Three free-roaming Victoria crowned pigeons (Goura victoria) housed in a completely enclosed tropical exhibit were found dead without antemortem signs of illness. The birds died within 9 days of each other. Gross necropsy revealed moderate pulmonary edema in all three birds. Histopathologic examination revealed pulmonary edema and pulmonary protozoal merozoites compatible with Sarcocystis spp., Toxoplasma gondii, or Neospora spp. infection. Immunohistochemical staining for T. gondii and Neospora spp. were negative. Immunohistochemical staining identified a Sarcocystis falcatula-like parasite in all three birds. It is suspected that new exhibit soil contaminated with feces from the Virginia opossum (Didelphis virginiana) was the source of the infective sporocysts.

Despite the extensive amount of research conducted on mourning doves (Zenaida macroura), no biochemical reference values exist for this species. Our objective, therefore, was to establish base line clinical chemistry reference values for mourning doves to assist with establishing clinical diagnoses. Wild mourning doves were captured 19 March 1996 to 8 August 1996, and 6 February 1998 to 12 May 1998; blood samples were collected from 382 mourning doves. Plasma biochemical values were established for glucose, sodium, potassium, chloride, enzymatic CO2, albumin, total protein, globulin, calcium, phosphorus, cholesterol, magnesium, aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), and uric acid. These reference values are invaluable for determining diagnosis of diseases of the gastrointestinal, hepatic, renal, cardiovascular, musculoskeletal, and endocrine systems.

Effects of feeding diets containing fumonisin B1 (FB1) and moniliformin (M), singly or in combination, on performance and immune response were evaluated in poults. Day-old poults were randomly assigned to one of four dietary treatments with four replicates of four poults each. Dietary treatments were 1) control; 2) 200 mg FB1, 0 mg M/kg diet; 3) 0 mg FB1, 100 mg M/kg diet; and 4) 200 mg FB1, 100 mg M/kg diet. In Experiment 1, poults were injected with 0.25 mL Newcastle disease virus (NDV) vaccine on Weeks 2 and 3 of the experiment, and anti-NDV antibody titers were measured 7 d after each injection. Compared with controls, poults fed FB1 had significantly lower (P < 0.05) secondary antibody response. Poults fed M and the combination of FB1 and M had significantly lower (P < 0.05) primary and secondary antibody response. Lower relative thymus weights were observed in poults fed diets containing FB1 or M. Decreased relative bursa and spleen weights were observed in poults fed M. In Experiment 2, poults were placed on dietary treatments for 3 wk. On Day 21, 2 x 10(6) peripheral lymphocytes were incubated with mitogens. Poults fed diets containing FB1 had a significantly lower (P < 0.05) proliferative response to mitogens in comparison to controls. In Experiment 3, poults were placed on the diets for 3 wk and were injected with 4.4 x 10(7) E. coli/kg body weight on Day 21. Significantly higher (P < 0.05) numbers of E. coli colonies were observed in the blood and tissue homogenates of poults fed M. In all three experiments, feed intake and body weight gains were significantly lower (P < 0.05) in turkeys fed diets containing M. Data from the present study suggest that FB1 and M are immunosuppressive in poults and that M not only suppresses immune response but also performance. However, neither synergistic nor additive effects between FB1 and M were observed for any of the parameters measured.

A poultry research facility that housed 2400 Peterson x Hubbard cross broilers (48 pens of 50 chicks each) experienced 4% mortality within 24 hr of chick placement. Mortality started within 4 hr of placement, and within 72 hr, cumulative mortality had reached 52%. Mild dyspnea was the only clinical sign noted in some chicks prior to death. The primary gross lesion noted in the chicks submitted was moderate to severe pulmonary congestion. The lungs of four of these chicks sank in formalin, and blood-tinged fluid was noted in the mouth and nares of two chicks. The microscopic lesions noted in the affected chicks were moderate to severe pulmonary edema and congestion. The diagnosis indicated to the submitter was that pulmonary edema caused by exposure to an unidentified noxious gas caused the death of the chicks. The poultry house environment was tested for sulfur dioxide, oxides of nitrogen, carbon monoxide, carbon dioxide, and volatile organic compounds (as produced by combustion engines); all tests were negative for significant levels of these compounds. A second broiler flock was placed in the same facility and the mortality at 6 wk was 11%, which was greater than the 2.5%-4.7% mortality seen in the previous four flocks on the farm. Further investigation revealed that the only change in management practice in this facility prior to the onset of the severe mortality problem was the replacement of 48 heat lamp bulbs (one for each pen). The new heat lamp bulbs were polytetrafluoroethylene (PTFE) coated. PTFE gas intoxication has been reported in several exotic avian species, but this intoxication has not been previously reported in a poultry flock.

Three trials were conducted to evaluate the effect of moniliformin (M) on performance and immune function in chicks. Day-old chicks were randomly assigned to four dietary treatments (0, 50, 75, or 100 mg M/kg diet). In Trial 1, chicks were placed on treatments for 3 wk and were injected intravenously with 4.6 x 10(6) Escherichia coli on Day 21. Blood samples were collected at 60, 120, and 180 min after inoculation, and liver, spleen, and lung were collected at 180 min postinjection. Compared with control chicks, chicks fed 75 and 100 mg M/ kg diet had higher (P < 0.05) numbers of E. coli colonies in the circulation, liver, and spleen. In Trial 2, chicks were placed on diets for 4 wk and were injected with 0.5 mL Newcastle disease virus (NDV) vaccine intramuscularly on Weeks 2 and 3 of the experiment. The primary and secondary anti-NDV antibody titers were measured 7 d after each injection. Chicks fed 100 mg M/kg diet had lower (P < 0.05) secondary antibody titers than did control chicks. In Trial 3, lymphocyte proliferation in chicks exposed to M in vivo and in vitro was determined. Results of the in vivo study showed that cell proliferation in response to mitogens from control- and M-fed chicks did not differ (P > 0.05). For the in vitro study, lymphocyte proliferation decreased linearly (P < 0.01) with increased concentrations of M. In all three trials, chicks fed 100 mg M/kg diet had lower (P < 0.05) feed intake and weight gain than did control chicks. Data from the current study suggested that M decreased performance and immune response in chicks at the level of 75 mg/kg diet.

Biogenic amines in spoiled animal by-product feeds have been implicated in causing poor performance and intestinal lesions in broilers. This study was designed to determine if biogenic amines, at the concentrations found in animal by-product meals, would reduce performance in broilers or cause lesions. Twelve treatments were used in a 2 x 6 factorial arrangement with the main effects being either a corn-soybean meal diet or a corn-soybean meal diet with 10% animal by-products added and either no amines added or added levels of phenylethylamine (4.8 mg/kg), putrescine (49 mg/kg), cadaverine (107 mg/kg), histamine (131 mg/kg), or a combination of all these amines. Levels of biogenic amines used in this study simulated those found in areas with reported problems attributed to biogenic amines. Broilers were monitored for performance, gross lesions, and histologic evidence of lesions at 2, 4, and 6 wk. No consistent effects were observed on performance, and by the conclusion of the trial, no statistical differences were noted in the performance of any of the treatments. No gross lesions were observed on a consistent basis in any of the treatments. Histopathology was likewise unremarkable. On the basis of this study, it would appear that these four biogenic amines, at levels detected in the United States, do not pose a serious health concern for the broiler industry.

The progeny of two emu breeder pairs, which had a history of producing offspring with gangliosidosis, were monitored for 15 mo. DNA fingerprinting revealed that individuals in each breeder pair were not related to each other. One breeder pair had 13 progeny that reached or exceeded the age of 1 mo, and six of these progeny developed gangliosidosis. The mean age at which these affected emus were euthanatized, with distinct neurologic disease, or died was 5.7 mo. The second emu pair had 13 progeny, seven of which developed gangliosidosis, with a mean age of euthanasia/death of 4.6 mo. Affected emus died or were euthanatized from 2 to 8 mo of age. The primary clinical sign in the affected emus was mild to severe ataxia. Severe hemorrhage into the body cavity or the muscles of the thigh was noted in 8 of 13 of the affected emus. Brain ganglioside levels were evaluated in six of the affected emus and six controls. Significant increases (P < 0.05) in gangliosides GM1 and GM3 were noted, with 2.3- and 4.9-fold increases in these two gangliosides, respectively, in affected emus. Furthermore, the diseased emu brains contained ganglioside GM2, whereas this monosialoganglioside was undetectable in the brains of normal controls. Total mean brain ganglioside sialic acid in affected emus was increased 3.3-fold in comparison with controls. Serum chemistries revealed elevated cholesterol and decreased uric acid levels in affected emus. Gangliosidosis in emus is an inherited disease process that, in the current study, caused 50% mortality in the progeny of two emu breeder pairs. The elimination of this lethal gene from emu breeder stock is essential for the long-term economic viability of the United States emu industry.

A previous study has demonstrated an unusual gangliosidosis in emu that is characterized by the accumulation of gangliosides in the brain tissues with GM3 and GM1 predominating. To provide insight into this unique disorder of emu gangliosidosis, the current study focused on analysis of neutral glycosphingolipids and gangliosides from brain and liver tissues of affected birds and healthy controls. We found not only that the total lipid-bound sialic acid content was increased three- and fourfold in the affected brain and liver, respectively, but also that the ganglioside pattern was rather complex as compared with the control. The absolute ganglioside sialic acid content was significantly increased in the diseased tissues, with the highest elevation levels of GM3 (14-fold) and GM1 (ninefold) in the affected brain. Relative increases in content of these monosialogangliosides were also significant. GM2 was only detected in the affected brain, but not in normal controls. The neutral glycosphingolipid fraction showed accumulation of many oligosylceramides, with six- and 5.5-fold increases in lactosylceramide levels for brain and liver, respectively. The level of myelin-associated galactosylceramide (GalCer) in the brain was decreased to only 41% of that in the healthy control, whereas no difference was found in liver tissues from both groups. Besides GalCer, the brain content of sulfatide (cerebroside-sulfate esters), another myelin-associated glycolipid, decreased to only 16% of the control. The loss of myelin-associated GalCer and sulfatide strongly suggests demyelination in the affected emu brain. Our overall data are consistent with the presence of a unique form of sphingolipidosis in the affected emus, perhaps with secondary demyelination, and suggest a metabolic disorder related to total sphingolipid activator deficiency.

Fumonisin B1 (FB1) and moniliformin (M) were supplied by Fusarium moniliforme M-1325 and Fusarium fujikuroi M-1214 culture material, respectively. Turkeys were fed a control ration, or rations containing 200 mg FB1/kg, 100 mg M/kg, or a combination of both 200 mg FB1/kg and 100 mg M/kg feed from 1 to 21 days of age. These rations contained 0, 3.8, 1.0, and 4.8% culture material, respectively. In comparison to controls, turkeys fed FB1 had increased relative liver weights. Both aspartate aminotransferase and lactate dehydrogenase were increased in poults fed FB1. Turkeys fed M had decreased feed intake and body weight gains and increased relative heart weights in comparison to controls. Poults fed FB1 had moderate diffuse hepatocellular hyperplasia and poults fed moniliformin had a loss of cardiomyocyte cross striations. Turkeys fed the ration containing both M and FB1 had all the above changes; however, no additive or synergistic effects were evident for any single parameter measured. No treatment-related morbidity or mortality was observed in the study.

An experiment was conducted with 180 female turkey poults to evaluate the effects of Fusarium fujikuroi M-1214 culture material, containing moniliformin (M), on turkey poults. Day-old female poults were allotted randomly to dietary treatments containing 0, 0.24, 0.48, 0.72, 0.96, 1.44, 1.92, 2.40 and 2.88% M culture material (MCM). These levels of MCM supplied 0, 25, 50, 75, 100, 150, 200, 250 or 300 mg M/kg of feed. Significant mortality occurred in poults fed 200 (six out of 20), 250 (nine out of 20) and 300 (nine out of 20) mg M/kg feed. Poults fed 100 mg M/kg or greater had lower (P<0.05) feed intakes than controls. Decreased body weight gains were observed in poults fed diets containing 100 mg M/kg or higher. In contrast, feed conversion was only affected (P<0.05) at dietary levels of 200 mg M/kg feed or higher. Increased heart weights (P<0.05) were observed in poults fed greater than or equal to 50 mg M/kg. Gross lesions of M toxicity were a generalized cardiomegaly. Histopathology revealed focally extensive to generalized loss of car-diomyocyte cross striations (granular change) and numerous large cardiomyocyte nuclei in poults fed greater than or equal to 50 and 100 mg M/kg, respectively. Results indicated that Fusarium fujikuroi culture material containing moniliformin at greater than or equal to 50 mg M/kg is toxic to turkey poults.

The effects of feeding Fusarium moniliforme culture material, containing known concentrations of fumonisin B1 (FB1), were studied in turkey poults. Day-old poults were allotted randomly to dietary treatments containing 0, 0.41, 0.82, 1.23, 1.64. 2.87, 4.10, 5.33, 6.56, and 7.79% fumonisin culture material (FCM). These levels of FCM supplied 0, 25, 50, 75, 100, 175, 250, 325, 400, and 475 mg FB1/kg of feed. Each dietary treatment was fed to six pen replicates of six poults each for 21 d. Poults fed FCM that supplied 325 to 475 mg FB1/kg diet had lower (P < 0.05) feed intakes and BW gains. Increased (P < 0.05) liver and pancreas weights were observed in poults fed FCM that supplied > or = to 175 mg FB1/kg. Poults fed FCM that supplied 400 and 475 mg FB1/kg diet had increased (P < 0.05) red blood cell counts and increased (P < 0.05) serum concentrations of gamma glutamyl transferase and aspartate aminotransferase. Compared with controls, poults fed FCM that supplied 25, and 75 to 475 mg FB1/kg had increased (P < 0.05) liver sphinganine:sphingosine ratios. Hepatocellular hyperplasia was mild at 75 and 100 mg FB1/kg diet, moderate to severe at 250 mg/kg FB1, and severe at 325 to 475 mg FB1/kg. Multifocal to generalized loss of cross striations and thinning of cardiomyocytes was observed in poults fed FCM that supplied 475 mg FB1/kg diet. Results indicated that diets containing < or = to 1.23% FCM that supplied > or = to 75 mg FB1 /kg are toxic to young turkeys.

Fourteen 1-day-old male turkeys were randomly assigned to two adjacent floor pens and fed balanced rations containing 0 and 75 mg fumonisin B1 (FB1)/kg for 18 weeks. Inclusion of FB1 in the ration caused decreased body weight gain on weeks 4, 10, and 12 during the trial. Turkeys fed 75 mg FB1/kg had significantly heavier livers after treatment for 18 weeks. Chronic FB1 exposure resulted in an increased total white blood cell count, absolute heterophil count, absolute lymphocyte count, and heterophil-to-lymphocyte ratio. No mortality was noted in turkeys in either treatment group. Turkeys are relatively resistant to chronic FB1 exposure.

Fusarium moniliforme culture material containing fumonisin B1 (FB1) was fed to white Pekin ducklings from 1 to 21 days of age. Four dietary treatments were prepared with 0, 100, 200, and 400 mg FB1/kg ration. Ducklings fed rations containing FB1 had a dose-dependent decrease in feed intake and weight gain. Increasing levels of FB1 in the ration were associated with increasing absolute organ weights of liver, heart, kidney, pancreas, and proventriculus. Liver sphinganine to sphingosine ratios increased significantly in ducklings fed FB1. Two of eight ducklings fed a ration containing 400 mg FB1/kg died prior to the termination of the experiment. Mild to moderate hepatocellular hyperplasia was evident in all ducklings fed FB1. Mild to moderate biliary hyperplasia was also noted in the liver sections of ducklings fed 400 mg FB1/kg in the ration. Ducklings, like other poultry, are relatively resistant to the toxic effects of FB1.

An eighteen-month-old female rhea (Rhea americana) was presented dead for necropsy. The owner reported having observed blood in the droppings. Gross examination revealed a rhea in good body condition with a copious amount of frank blood in the cloaca. Large masses of matted fescue grass (Festuca spp.) distended the ventriculus and jejunum. No hemorrhage was evident in the digestive tract, which was otherwise void of ingesta. The kidneys were dark brown in color. Renal histopathology revealed a severe accumulation of eosinophilic pigment in the tubular epithelial cells of the proximal convoluted tubules, with tubular nephrosis and eosinophilic casts in the collecting tubules. It was concluded that the renal pigment was hemoglobin and not myoglobin, based on lack of evidence of muscle injury and the severe erythrophagocytosis evident in hepatic macrophages. The renal pigment also stained positive with the hemoglobin-specific Okajima stain. Hemoglobinuric nephrosis has not previously been reported in an avian species.

A 6-month-old female emu (Dromaius novaehollandiae) died following acute central nervous system signs. Hematoxylin-and-eosin-stained sections revealed that neurons of the brain were distended with nonstaining 1-to-2-microns vacuoles. Ultrastructural examination of the affected neurons revealed numerous membranous cytoplasmic bodies (MCBs) similar in appearance to the MCBs seen in mammalian gangliosidoses. A full sibling of this emu was donated for study. This 7-month-old female emu was stunted compared with hatchmates. Neurologic examination revealed hypermetric gait, persistent head tremor, and mild ataxia. No gross lesions were evident at postmortem. Histopathologic and electron microscopic findings were similar to those in the index case in that swollen, pale neurons were present in the cerebrum, pons, medulla, cerebellum, spinal cord, spinal ganglia, autonomic ganglia, myenteric plexus, and ganglion cell layer of the retina. Analysis of brain gangliosides of the affected 7-month-old emu revealed 14- and 25-fold increases of GM1 and GM3 gangliosides, respectively, compared with control emus. The total brain ganglioside sialic acids were, on a wet weight basis, 519 micrograms/g (control A), 658 micrograms/g (control B), and 1800 micrograms/g (affected emu). The familial association seen with this condition suggests that emus are affected by an inherited disorder similar to mammalian gangliosidoses.

An experiment was conducted with 270 male broiler chicks to evaluate the effects of a Fusarium fujikuroi M-1214 culture material containing moniliformin (M) on broiler chicks. Day-old chicks were allotted randomly to dietary treatments containing 0, .24, .48, .72, .96, 1.44, 1.92, 2.40, and 2.88% M culture material (MCM). These levels of MCM supplied 0, 25, 50, 75, 100, 150, 200, 250, or 300 mg M/kg of feed. Each dietary treatment was fed to six pen replicates of five chicks per pen for 21 d. Significant mortality (P < .05) occurred in chicks fed 200 (8 out of 30), 250 (17 out of 30), and 300 (25 out of 30) mg M/kg feed. Chicks fed > 100 mg M/kg had lower (P < .05) feed intakes and smaller BW gains (P < .05) than controls. Increased heart weights (P < .05) were observed in chicks fed > 50 mg M/kg, and increased liver weights (P < .05) in chicks fed > 100 mg M/kg. Gross lesions of M toxicity included generalized cardiomegaly with dilation of the right ventricle. Histopathology revealed a high incidence of large and variably shaped cardiomyocyte nuclei and a generalized loss of cardiomyocyte cross striations in chicks fed > 75 and 200 mg M/kg, respectively. Results indicated that F. fujikuroi culture material containing M is toxic to young broiler chicks.

The effects of feeding Fusarium moniliforme M-1325 culture material (CM), grown under different environmental conditions, were studied in turkey poults. Poults were fed a control diet or diets containing four levels of FB1 (75, 150, 225, or 300 mg/kg) prepared from F. moniliforme M-1325 cultures that produced 7800 (CM1) or 4000 mg FB1/kg (CM2). F. moniliforme M-1325 CM that produced a low concentration of FB1 (350 mg FB1/kg) was also used to prepare an additional diet containing 75 mg FB1/kg (CM3). Dose-dependent decreases in feed intake and body-weight gains and dose-dependent increases in liver weights and serum sphinganine (SA) to sphingosine (SO) ratios were observed in poults fed CM1 or CM2. Poults fed CM3 consumed more feed and had lower body-weight gains than controls or poults fed CM1 or CM2 (at 75 mg FB1/kg). Poults fed CM3 also had increased liver weights and SA:SO ratios compared with control poults. Generalized hepatocellular hyperplasia was observed in all FB1 treatment groups. Biliary hyperplasia was evident in turkeys fed 150 to 300 mg FB1/kg. Results indicate that at equivalent dietary FB1 levels, F. moniliforme cultures producing different concentrations of FB1 differ in their effects on turkey poults.

The individual and combined effects of fumonisin B1 (FB1) and aflatoxin B1 (AF) were evaluated using a 2 x 2 factorial with treatments of 0 and 75 mg FB1/kg feed and 0 and 200 micrograms AF/kg feed. Each of the four diets was fed to eight pen replicates of six poults from Day 1 to 21. Body weight gain was reduced (P < .05) by AF and the FB1-AF combination. Poults fed AF or the FB1-AF combination were less efficient (P < .05) in converting feed to gain. Fumonisin B1 increased (P < .05) liver weights whereas AF and the FB1-AF combination increased (P < .05) spleen weights. The AF and the FB1-AF combination decreased (P < .05) serum concentrations of albumin, total protein, and cholesterol. Fumonisin B1 and the FB1-AF combination increased (P < .05) serum sphinganine:sphingosine (SA:SO) ratios. Treatment-associated lesions were observed only in the liver. Hepatocellular hyperplasia and biliary hyperplasia were seen in poults fed 75 mg FB1/kg and 200 micrograms AF/kg, respectively. The combination of FB1 and AF caused an increased primary immune response to sheep red blood cells. However, the phytohemagglutinin delayed hypersensitivity response was not affected by dietary treatment. These data indicate that FB1 and AF, alone and in combination, can adversely affect poult performance and health at these dietary concentrations.

Two groups of 100 white leghorn hens were fed rations either supplemented or deficient in vitamin A for 32 weeks. At the conclusion of the study, vitamin A-supplemented hens laying normally were also compared with a group of vitamin A-supplemented hens in a state of low egg production. Mean egg retinol equivalents (microgram retinol/g egg yolk), egg production, and hatchability in the vitamin A-deficient group were decreased significantly by 4, 20, and 28 weeks, respectively, after beginning treatment. The ovaries of vitamin A-deficient chickens had increased numbers of atretic follicles compared with the ovaries of vitamin A-supplemented hens (20, 24, 28, and 32 weeks), and these atretic follicles contained moderate to severe hemorrhage. Hemorrhage was located either uniformly throughout the follicle or more commonly between the detached granulosa cell layer and the theca interna. Hemorrhagic follicles were uncommon in both vitamin A-supplemented hens and low-production vitamin A-supplemented hens.

The effects of feeding Fusarium moniliforme culture material, containing known concentrations of fumonisin B1 (FB1), were studied in broiler chicks. Day-old chicks were allotted randomly to dietary treatments containing 0, 1.02, 2.04, 3.06, 4.08, 5.10, 6.12, and 7.14% fumonisin culture material (FCM). These levels of FCM supplied 0, 75, 150, 225, 300, 375, 450, and 525 mg of FB1/kg of feed. Each dietary treatment was fed to four pen replicates of six birds each for 21 days. Chicks fed FCM that supplied 450 and 525 mg FB1/kg diet had lower (P < .05) feed intakes and BW gains; increased (P < .05) liver and kidney weights; and increased (P < .05) mean cell hemoglobin, and mean cell hemoglobin concentrations. Compared with controls, chicks fed FCM had increased (P < .05) free sphinganine levels and sphinganine:sphingosine ratios. Treatment-associated histological lesions were only observed in the liver of chicks fed diets containing FCM that supplied 225 mg FB1/kg or higher. Diets containing FCM that supplied levels as low as 75 mg FB1/kg affected the physiology of chicks by increasing free sphinganine levels and sphinganine:sphingosine ratios. Because inhibition of sphingolipid biosynthesis has been hypothesized as the mechanism of action of FB1, this suggests that diets containing 75 mg FB1/kg FCM may be toxic to young broiler chicks.

Feces-stained eggshells, diarrhea, and typhlitis were identified in two commercial laying flocks in Ohio. Hens with diarrhea had spirochetes in cecal lumina and crypts. On culture, the spirochetes were motile and non-hemolytic, did not produce indole, had 12 to 15 axial filaments, were 9.2 to 11.7 microns in length and 240 to 370 nm in diameter, and had a wavelength of 5.1 to 6.5 microns on transmission electron microscopy.

A flock of 5000 six-week-old bobwhite quails (Colinus virginianus) experienced high mortality (52%) over a 2-day period. Mortality was 99% within a 6-day period. Clinical signs were depression followed shortly by death. Gross lesions observed in dead quails were congested lungs and, in a few cases, mottled livers. Histopathologic examination revealed severe, diffuse, heterophilic interstitial pneumonia and multifocal areas of hepatic and splenic necrosis with numerous intracellular and extracellular short bacterial rods. Serotype 3, 4, 15, 16, Pasteurella multocida, isolated from the index case, caused 50% mortality in experimentally inoculated bobwhite quails within 9 to 24 hours. This report indicates that pasteurellosis can cause peracute disease in bobwhite quails with very high mortality.

Two radiopharmaceuticals, technetium 99m-N-(2-mercapto-1-oxopropyl)glycine (99mTc-I) and technetium 99m-ethylenediamine-N,N'-bis(alpha-2-hydroxy-5-bromophenyl)acetic acid (99MTc-II), were prepared and evaluated in dogs, rabbits, and rats. Both agents gave good scintigraphic images of the liver and gallbladder in dogs. The cumulative amount of 99mTc-I and 99mTc-II excreted in the bile of dogs and the physiological disposition data in rats revealed slight, inconclusive differences in their distributions. However, the scintigraphic images and physiological disposition data in rabbits revealed gross differences in the distribution pattern of the two agents. The observed similarities in the biliary excretion of both agents in dogs and rats were attributed to the fact that these species are relatively good biliary excretors, and both agents therefore were excreted extensively. However, rabbits, which are poor biliary excretors relative to dogs and rats, excreted 99mTc-II more extensively than 99mTc-I because of the favorable molecular characteristics of 99mTc-II.

Cryptosporidium meleagridis oocysts, originally isolated from droppings of commercial turkey poults with increased mortality due to viral (reovirus) hepatitis and enteritis, were treated with peracetic acid to kill companion bacteria and viruses and then propagated by passage in young turkeys. Thirty-eight 5-day-old large white turkey poults were inoculated by crop gavage with 500,000 cryptosporidial oocysts and compared with 40 uninoculated poults. Cryptosporidial oocysts shedding began 3 days postinoculation (PI), peaked on day 4 PI, and persisted at a low level for the duration of the 21-day trial. Low to moderate cryptosporidial infections of the ileal mucosa (days 3, 6, and 15 PI), cecal mucosa (days 3, 6, and 21 PI), and bursa of Fabricius (days 6, 12, 15 and 21 PI) were found on histopathological examination. There were no differences in mean body weights between the inoculated and uninoculated groups, and no mortality or clinical signs of disease were seen in either group.

Six derivatives of ethylenediamine-N,N'-bis (alpha-2-hydroxy phenyl) acetic acid labeled with technetium 99m were prepared and their imaging qualities evaluated in ponies. The 6 agents produced good scintigraphic images of certain structures of the liver in the pony. For each agent, 13 different scans were taken. Dorsal views of the left lateral, right lateral, and quadrate lobe were obtained with dorsal scans. Left lateral and left lateral oblique (45 degrees) scans provided a left lateral view of the left lobe and a medial view of the right lateral lobe. Right lateral scans revealed the right lateral and quadrate lobes. Administration of 99mTc-labeled colloids which are commonly used in other species for liver scintigraphy resulted in extensive lung uptake in the pony.

We present the case of a 28-year-old man being treated with Nardil for chronic depression who developed a hypertensive crisis and a severe occipital headache one hour after ingesting an over-the-counter appetite suppressant. The adverse reactions between MAO inhibitors and phenylpropanolamine and discussed, as are the dangers of using Demerol to treat the headache and Aldomet to treat the hypertension.