Search PubMed⌕ Search

Biomedical subjects

M D Ficken

Publications and source records attributed to M D Ficken.

36 records · Page 2Linked to original sources

Cryptosporidiosis and turkey viral hepatitis in turkeys.

Cryptosporidiosis and turkey viral hepatitis were diagnosed in 25-day-old turkeys with increased mortality, enteritis, and stunting. Necropsy lesions included foul-smelling, tan-colored, loose feces in the terminal small intestines and ceca. The small intestines and ceca were congested. Multiple white to gray foci were present in the liver and pancreas. Mortality attributed to these conditions was estimated at 4.9%. Microscopic lesions included necrosis with accumulations of macrophages in the liver and pancreas. Bile-duct hyperplasia was present in the livers. Microscopic intestinal lesions consisted of mild to moderate atrophy of the villi of the distal small intestine (ileo-cecal junction) with infiltration of the lamina propria by mononuclear cells. Cryptosporidia were identified and appeared to be attached to villous epithelial cells of the terminal small intestines. Cryptosporidium sp. oocysts were also confirmed by fluorescent microscopic examination of feces stained auramine O. Reovirus was isolated on chicken embryo liver cells from affected livers.

Animals↗

Intestinal and bursal cryptosporidiosis in turkeys following inoculation with Cryptosporidium sp. isolated from commercial poults.

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.

Animals↗

Skeletal muscle lesions in turkeys associated with the feeding of monensin.

The feeding of monensin as a coccidiostat in three separate flocks of turkeys was associated with increased mortality, posterior paresis, and a skeletal muscle myopathy. Mortality attributed to the disease was 1.65%, 1.86%, and 4.80% in the three flocks. Samples of monensin-supplemented feed fed to the flocks when showing clinical signs contained 88, 85, and 106 g/ton of complete feed, respectively. Clinically, the turkeys showed posterior paresis, inability to rise, incoordination, reluctance to move, and leg trembling and weakness. Necropsy findings included consistent lesions of pallor within the type I muscles of the legs, wings, and backs. Microscopic lesions included myofiber degeneration and necrosis with massive cellular proliferation interpreted as sarcolemmal nuclei proliferation. Occasional axonal degeneration with loss of axons was present in peripheral nerves embedded in the damaged musculature. In the youngest flock, multifocal areas of acute coagulation necrosis of the myocardium were also present. These outbreaks occurred following intake of monensin in the complete feed at levels considered therapeutic; however, no associated predisposing clinical condition, drug/toxin interaction, or excessive monensin levels in the feed could be demonstrated.

Animals↗

Effect of cyclophosphamide on selected hematologic parameters of the turkey.

The effect of three daily cyclophosphamide (CY) injections (doses of 0-100 mg/kg.day) on selected hematologic parameters in 7-to-8-week-old female Nicholas turkeys was examined. CY induced significant leukopenia, lymphopenia, thrombocytopenia, and heteropenia 24 to 72 hours after the initial injection; time depended on cell type and dose of CY. Significant linear correlation between increasing CY dose and increasing severity of circulating cell depression occurred. CY had no significant effect on circulating numbers of monocytes, packed cell volume, or plasma protein. Changes in basophils and eosinophils could not be identified because of their low numbers.

Animals↗

Tracheal mucus transport rate and bacterial clearance in turkeys exposed by aerosol to La Sota strain of Newcastle disease virus.

Tracheal mucus transport rate (TMTR) and quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sac were measured in healthy unanesthetized turkeys and in turkeys exposed by aerosol to a La Sota vaccine strain of Newcastle disease virus (NDV). The TMTR of uninfected turkeys was 42.4 +/- 14.7 cm/min. The TMTR of NDV-infected turkeys was depressed on days 3 through 7 postexposure (PE); depression was significant (P less than or equal to 0.05) on day 7 PE. Tracheal E. coli clearance in NDV-infected turkeys was reduced on days 4 through 9 PE, significantly so on day 5 PE (P less than or equal to 0.01). Depression of TMTR and tracheal E. coli clearance were associated histologically with replacement of normal pseudostratified columnar epithelium by 3 to 8 layers of immature nonciliated cells. E. coli clearance by the lung and air sac of NDV-infected turkeys was depressed on days 5 through 9 PE.

Air Sacs↗

Staphylococcus-induced gangrenous dermatitis in broilers.

An infectious bursal disease (IBD)-vaccinated flock of 23,900 broilers, 17 days of age, experienced sudden onset of depression, dermatitis, and mortality. Postmortem examination showed extensive subcutaneous serosanguineous fluid accumulation over the pectoral muscles, discrete hepatic whitish foci, fluid-filled intestines, and small, flaccid bursae of Fabricius. Gram-stained impression smears from the affected areas revealed numerous gram-positive cocci. Aerobic culture of liver and subcutaneous tissue consistently produced heavy growth of penicillin-sensitive Staphyloccus aureus. Histopathologically, subcutaneous tissue showed diffuse hemorrhage and large numbers of gram-positive cocci with severe congestion and hemorrhage of the underlying skeletal muscle. Liver sections showed multiple, randomly scattered areas of acute coagulation necrosis with numerous gram-positive cocci. Bursal lesions were characterized by extensive follicular necrosis and collapse. A diagnosis of staphylococcal gangrenous dermatitis secondary to IBD was made. Mortality returned to preinfection levels within 72 hours after penicillin was added to the drinking water.

Animals↗

Effects of Newcastle disease virus infection on the binding, phagocytic, and bactericidal activities of respiratory macrophages of the turkey.

Effects of Newcastle disease virus (NDV) infection on the binding, phagocytic, and bactericidal activities of turkey respiratory macrophages were studied. Respiratory macrophages of the turkey demonstrated the presence of immunoglobulin (Ig) G and complement receptors but lacked IgM receptors. Respiratory macrophages from NDV-infected turkeys showed little or no depression of binding of sheep erythrocyte-IgG complexes and sheep erythrocyte-IgM-complement complexes to their appropriate membrane receptors. In contrast, respiratory macrophages from NDV-infected turkeys showed significant (P less than or equal to 0.05) depression of phagocytosis of similar complexes. Bacterial killing by respiratory macrophages from NDV-infected turkeys was significantly (P less than or equal to 0.05) inhibited.

Animals↗

Clearance of bacteria in turkeys with Bordetella avium-induced tracheitis.

Quantitative clearance of aerosolized Escherichia coli from the trachea, lung, and air sacs was measured in turkeys infected with Bordetella avium. Clearance of E. coli in turkeys with B. avium-induced tracheitis was minimally affected early in infection. Sixteen to 23 days after infection with B. avium, sporadic, mild depressions in clearance of E. coli were observed in the tracheas, which had large areas of deciliated tracheal epithelium or replacement of normal epithelium by immature hyperplastic epithelium or metaplastic squamous epithelium. Clearance of E. coli from the lung and air sacs was minimally affected in turkeys infected with B. avium.

Animals↗

Tracheal mucus transport rate in normal turkeys and in turkeys infected with Bordetella avium (Alcaligenes faecalis).

Using the radiopharmaceutical 99mtechnetium-sulfur colloid, the tracheal mucus transport rate (TMTR) was measured in healthy unanesthetized turkeys and in turkeys infected with Bordetella avium. The TMTR of uninfected turkeys was 35.6 +/- 14.4 cm/min. The TMTR of B. avium-infected turkeys was normal on days 0 through 14 postexposure (PE), despite heavy bacterial colonization of the tracheal epithelium. On day 21 PE, the TMTR of B. avium-infected turkeys was significantly depressed (P less than or equal to 0.01) compared with that of control turkeys. Depressed transport was associated with extensive loss of ciliated epithelium from the tracheal mucosa and replacement of the normal mucosa by immature nonciliated epithelium or metaplastic squamous epithelium.

Alcaligenes↗

Induction, collection, and partial characterization of induced respiratory macrophages of the turkey.

Respiratory macrophages (RM) of the turkey were elicited with a 1:4 (v/v) suspension of incomplete Freund's adjuvant in sterile phosphate-buffered saline injected directly into the abdominal air sacs. RM were purified by passage through a Ficoll-Hypaque gradient resulting in 95.7 +/- 5.9% purity and 94.8 +/- 12.3% viability. On days 7 and 9 postinjection, adequate numbers (7.15 +/- 5.47 X 10(6) macrophages per turkey) of RM for in vitro experiments were obtained. RM of the turkey demonstrated the ability to adhere to glass, phagocytize Zymosan A, and kill Escherichia coli in vitro.

Animals↗

Antibiotic aerosolization for treatment of alcaligenes rhinotracheitis.

Aerosolization of oxytetracycline hydrochloride for treatment and control of rhinotracheitis caused by Alcaligenes faecalis was performed in complete confinement on two turkey flocks immediately preceding vaccination with Newcastle disease virus (NDV). Tracheal culture results indicated populations of A. faecalis decreased following treatment. Clinical observations showed the treated turkeys had greater activity and more alertness compared with untreated A. faecalis-infected flocks, and respiratory sounds were diminished overall. Increased food and water consumption and no stunting was observed in treated turkeys. Treated flocks had a substantial decrease in mortality during the 4-week post-NDV vaccination period compared with untreated flocks. These results, although inadequately controlled, suggest a promising treatment program for A. faecalis infection in turkeys.

Aerosols↗

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↗

Decreased egg production in turkeys experimentally infected with eastern equine encephalitis virus or Highlands J virus.

Turkey breeder hens were experimentally infected with strains of eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus previously isolated from turkey hens experiencing decreased egg production. Depression and inappetance were observed on day 1 postexposure (PE) in hens inoculated with either EEE virus or HJ virus, and egg production fell in each virus-inoculated group from approximately 75% to less than 20% within 2-3 days PE. Egg production remained depressed (less than 20%) for 15 days in EEE-virus-inoculated hens and for 7 days in HJ-virus-inoculated hens. EEE virus and HJ virus were recovered from various tissues on days 1-5 PE, and virus was detected in eggs laid on days 2-5 PE. The findings of this study confirm that EEE virus and HJ virus are potential causes of decreased egg production in turkey breeder hens.

Alphavirus Infections↗

Effect of protein restriction during brooding on spontaneous turkey cardiomyopathy.

The effect of early protein restriction on poult performance and mortality due to spontaneous turkey cardiomyopathy were examined in a facility that historically had a high incidence of the condition. Two thousand male turkey poults were divided into two equal subgroups for the first 4 weeks of life: one received standard commercial rations for the first 4 weeks (high-protein subgroup), and the other received rations with a protein content approximately 70% of the first subgroup (low-protein subgroup). Rations were the same after 4 weeks of age (standard commercial rations). At 16 weeks of age, turkeys in the low-protein subgroup weighed an average of 12.32 kilograms (27.1 pounds), whereas turkeys in the high-protein subgroup weighed an average of 12.73 kilograms (28.0 pounds). Total mortality for the low-protein subgroup was 10.1%, whereas total mortality for the high-protein subgroup was 15.7%. Total mortality due to spontaneous turkey cardiomyopathy in the high-protein subgroup was greater than twice that in the low-protein subgroup (10.4% versus 4.6%). These results show that lowering the protein content of the feed in the first 4 weeks significantly reduces mortality due to spontaneous turkey cardiomyopathy, but body weight gain is also reduced.

Animals↗

Egg-production drop in turkeys associated with alphaviruses: eastern equine encephalitis virus and Highlands J virus.

Alphaviruses were isolated from tracheas of turkey breeders in two North Carolina flocks experiencing a severe drop in egg production. Highlands J virus was isolated from one of the breeder flocks, in which production decreased by as much as 72.6% in selected houses over a 48-to-96-hour period. Eastern equine encephalitis virus was isolated from the second breeder flock, which experienced an egg-production drop of 44.5%. Clinical signs in both flocks were similar, with inactivity and the egg-production drop being the only clinical signs observed. Eggs from affected breeders were small and white, and a few were soft-shelled. Sera collected from the flocks 2 to 3 weeks after production began dropping confirmed the presence of antibodies to the viruses recovered. In the first flock, egg production failed to return to above 50%, although heat stress may have played a role in production recovery. The second flock was taken out of production and recycled.

Alphavirus↗

Cerebral encephalomalacia in commercial turkeys.

A flock of 9 1/2-week-old commercial tom turkeys experienced high mortality after consuming a complete feed containing an unidentified toxic substance. Initially, turkeys were found dead. Clinically, the birds were calm and still but became hyperexcitable with noise. A small percentage of birds exhibited torticollis, opisthotonos, circling, ataxia, and blindness. Findings at necropsy and upon microscopic examination were bilaterally symmetrical areas of necrosis of the cerebral hemispheres in the area of the neostriatum that were well demarcated from the surrounding normal neuropil. A feeding trial with the suspect feed in twelve 4-week-old turkey hens induced clinical disease and gross and microscopic brain changes similar to those observed in the field case. Analyses for the following substances in the suspect feed were either negative or within acceptable limits: salt, selenium, furazolidone, monensin, amprolium, 3-nitro-4-hydroxyphenylarsonic acid, aflatoxin, deoxynivalenol, zearalenone, T-2 toxin, ochratoxin, fumonisin, organophosphates, chlorinated hydrocarbons, and carbamates. The toxic component of the feed remains unidentified.

Animal Feed↗

Experimental infection of young turkeys with eastern equine encephalitis virus and highlands J virus.

Depression, somnolence, and increased mortality were observed in 2-week-old turkeys inoculated intramuscularly with either eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus. Mortality rates in EEE virus- and HJ virus-inoculated turkeys were 7/30 (23%) and 9/30 (27%), respectively; no sham-inoculated controls died. Both EEE virus- and HJ virus-inoculated turkeys developed viremia that lasted 2 days; peak mean titers were 5.5 and 3.2 log10 plaque-forming units per ml of blood, respectively. Pathologic changes in both EEE virus- and HJ virus-inoculated turkeys consisted primarily of multifocal necrosis in the heart, kidney, and pancreas, and lymphoid necrosis and depletion in the thymus, spleen, and bursa of Fabricius. The findings indicate that EEE virus and HJ virus are pathogenic for young turkeys.

Alphavirus↗

High mortality of domestic turkeys associated with Highlands J virus and eastern equine encephalitis virus infections.

High mortality occurred in two flocks of commercial turkey hens placed in southern North Carolina in fall 1991. Daily mortality peaked at 3.19% in Flock 1 and 3.79% in Flock 2. Clinical signs included restlessness, somnolence, vocalization, and acute death. Gross lesions included atrophy of the bursa of Fabricius, thymus, and spleen, and watery intestinal contents. Microscopic changes included moderate to marked lymphocyte necrosis and depletion in the bursa, thymus, and spleen, widely scattered necrosis of pancreatic acinar cells, and mild villous atrophy and fusion in the jejunum and ileum with cuboidal to low columnar epithelial cells covering the villous tips. In Flock 1, at 27 days of age, reovirus and picornavirus particles were detected in the feces. One week later, togavirus-like particles were observed in fecal contents, and two of seven serum samples showed seroconversion to Highlands J virus. Eleven days later, five of six serum samples were positive for antibodies against Highlands J virus, with a fourfold increase in the geometric mean titer. In Flock 2, seroconversion to eastern equine encephalitis virus was observed in four of 10 serum samples 11 days after the onset of clinical signs. Based on the above observations, it is suspected that these alphaviruses were the cause of the clinical syndrome.

Alphavirus↗