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Biomedical subjects

M D Ficken

Publications and source records attributed to M D Ficken.

At least 19 recordsLinked to original sources
PubMed1992

Acute airsacculitis in untreated and cyclophosphamide-pretreated broiler chickens inoculated with Escherichia coli or Escherichia coli cell-free culture filtrate.

Ninety commercial broiler chickens were divided into three equal groups; 30 were injected with brain-heart-infusion broth into the cranial thoracic air sacs (controls), 30 were similarly inoculated with a culture of Escherichia coli, and 30 were similarly inoculated with E. coli cell-free culture filtrate. Birds were examined from 0 to 6 hours post-inoculation. E. coli-inoculated and cell-free culture filtrate-inoculated chickens reacted similarly, with exudation of heterophils into the air sac. Microscopically, heterophils were present in low numbers perivascularly 0.5 hour after inoculation and became more numerous by 3 hours post-inoculation. By 6 hours post-inoculation, there was severe swelling of air sac epithelial cells and thickening of the air sac by proteinaceous fluid and heterophils. Ultrastructurally, air sac epithelial cells were swollen and vacuolated, and interdigitating processes were separated. Histologically and ultrastructurally, all features in control chickens were normal, with only rare heterophils in the air sac interstitium. In E. coli-inoculated and cell-free culture filtrate-inoculated chickens, cell counts (predominantly heterophils) in air sac lavage fluids increased markedly at 3 and 6 hours, with only slight increases in counts from lavages of controls. Heteropenia was observed in E. coli-inoculated chickens, whereas heterophilia was observed in cell-free filtrate chickens and controls. Ninety additional chickens were pretreated with cyclophosphamide, subdivided into three equal groups, and inoculated and examined similarly as above. Cyclophosphamide pretreatment reduced inflammatory changes in air sacs, lowered cell numbers in lavage fluids, and abolished hematologic changes; however, it did not prevent epithelial cell changes. These results indicate that cell-free culture filtrate of E. coli induces changes similar to those induced by cultures of E. coli.

Acute Disease↗
PubMed1991

Acute airsacculitis in turkeys inoculated with cell-free culture filtrate of Pasteurella multocida.

Twenty-six female and 26 male turkeys, inoculated into the caudal thoracic air sacs with cell-free culture filtrate of Pasteurella multocida strain R44/6, were examined from 0 to 6 hours post-inoculation and compared with 26 female and 26 male sham-inoculated control turkeys given brain-heart-infusion broth. The air sac reacted rapidly with exudation of heterophils. Microscopically, low numbers of heterophils were present within air sac blood vessels and also perivascularly by 0.5 hour after inoculation. These became more numerous by 1.5 and 3 hours post-inoculation. By 6 hours post-inoculation, there was severe swelling of air sac epithelial and mesothelial cells and thickening of the air sac by proteinaceous fluid and heterophils. Ultrastructurally, mesothelial and air sac epithelial cells were vacuolated, and interdigitating processes of epithelial cells were separated. Microscopically, in control turkeys, rare heterophils were present perivascularly at 1.5, 3, and 6 hours after inoculation. Ultrastructurally, all features were normal. In turkeys given cell-free culture filtrate, total cell counts in air sac lavage fluids increased markedly by 3 hours post-inoculation in which heterophils predominated (greater than 97%). There were only slight increases in cell counts of air sac lavages from control turkeys. The circulating blood heterophil cell count dropped transiently at 1.5 hours post-inoculation, followed by a return to normal 3 hours after inoculation, and by heterophilia by 6 hours post-inoculation in turkeys given either cell-free culture filtrate or brain-heart-infusion broth. These results indicate cell-free culture filtrate of P. multocida induces hematologic, cytologic, and morphologic changes indistinguishable from those induced by cultures of P. multocida.

Acute Disease↗
PubMed1991

Non-surgical cannulation of the vena cava for chronic blood collection in mature swine.

A nonsurgical cannulation technique for blood collections from mature swine was evaluated. Primiparous Yorkshire-Landrace sows (n = 6) received an indwelling jugular vein cannulae for 7 days duration. Recannulation was performed at monthly intervals for a total of 14 months. During cannulation, sows were restrained in a standing position using a rope snout snare. A 12-gauge by 10 cm needle was inserted into the jugular vein. Sterilized polyvinyl chloride tubing was advanced through the needle into the vein and a blunted 18-gauge needle and attached intermittent injection hub was inserted into the free end of the tubing. Surgical tape was used to form a butterfly on the tubing by suturing the tape to the animals' skin. Foam padding, livestock cement, and elastic tape helped to keep the tubing in position. Problems with cannulae patency and maintenance were few. No behavioral problems or systemic signs of illness were noted and necropsy examinations performed after the final cannulation revealed few abnormalities associated with chronic intermittent cannulation. This technique provides a safe, quick, effective means for multiple and repeated cannulae placement for blood collection from mature swine with minimal effects on the animal and without the risks associated with surgical techniques.

Animals↗
PubMed1990

Establishment and characterization of a chicken mononuclear cell line.

A new chicken mononuclear cell line (MQ-NCSU) has been established. The starting material used to initiate this cell line was a transformed spleen from a female Dekalb XL chicken which had been experimentally challenged with the JM/102W strain of the Marek's disease virus. After homogenization, a single cell suspension of splenic cells was cultured using L.M. Hahn medium supplemented with 10 microM 2-mercaptoethanol. Under these culture conditions, a rapidly proliferating cell was observed and then expanded after performing limiting dilution cultures. These cells were moderately adherent and phagocytic for sheep red blood cells and Salmonella typhimurium. When tested against a panel of monoclonal antibodies (mAb) using the flow cytometry, MQ-NCSU cells stained readily with anti-chicken monocyte specific (K-1) mAb but did not stain with mAb detecting T-helper, T-cytotoxic/suppressor, and NK cells. MQ-NCSU cells expressed very high levels of Ia antigens and transferrin receptors. In addition, cell-free supernatant obtained from MQ-NCSU culture contained a factor which exhibited cytolytic activity against tumor cell targets. Based on their cultural, morphological, and functional characteristics and mAb reactivity profile, we conclude that MQ-NCSU cell line represents a malignantly-transformed cell which shares features characteristic of cells of the mononuclear phagocyte lineage.

Animals↗
PubMed1990

Acute airsacculitis in turkeys inoculated with phorbol myristate acetate.

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.

Air Sacs↗
PubMed1989

Acute airsacculitis in turkeys inoculated with Pasteurella multocida.

Thirty female turkeys, inoculated into the caudal thoracic air sacs with Pasteurella multocida were examined from 0 to 6 hours post-inoculation (PI). The air sac reacted rapidly and intensely with exudation of heterophils. Circulating leukocyte and thrombocyte numbers remained normal except for an absolute lymphopenia by 6 hours PI. P. multocida was initially isolated from blood at 3 hours PI. Total cell counts increased markedly in air sac lavage fluids by 1.5 hours PI and continued to increase until 6 hours PI. Heterophils predominated in lavage fluids (greater than 94%), with macrophages comprising the remaining cells. Microscopically occasional heterophils were present within air sac blood vessels and perivascularly by 0.5 hour PI. They became more numerous by 1.5 and 3 hours PI when transepithelial migration into the air sac lumen was seen. By 6 hours PI, there was diffuse, severe swelling of air sac epithelium and mesothelium, and bacteria were located in air sac interstitium. Ultrastructurally, endothelial and air sac epithelial cells were swollen and vacuolated Interdigitating processes of air sac epithelial cells were separated. These results indicate that air sacs can be the portal of entry for P. multocida into the systemic circulation, probably via damaged air sac epithelium.

Air Sacs↗
PubMed1989

Histomoniasis and reticuloendotheliosis in a wild turkey (Meleagris gallopavo) in North Carolina.

A moribund wild turkey (Meleagris gallopavo) died shortly after it was discovered in Martin County, North Carolina (USA). The 4.3-kg female turkey appeared in good condition with no visible external lesions or evidence of injury. There were 2- to 5-mm yellow-white plaques on the mucosal surfaces of the oral cavity and mid-esophagus. The liver had large, multifocal, irregular pale areas on cut and uncut surfaces. The spleen contained multifocal, pale, hard, nodules. Microscopic changes in the liver consisted of large multifocal coalescing areas of necrosis. Occasional spherical 10 to 15 microns in diameter organisms consistent with Histomonas meleagridis were present in the necrotic areas. Viable hepatic parenchyma contained multifocal infiltrations of numerous mononuclear cells interpreted as neoplastic cells resembling lymphoblasts and plasma cells. Similar neoplastic cell infiltrates, consistent with the lymphoproliferative disease reticuloendotheliosis, were present in spleen, lung, and esophageal and oral mucosa. Reticuloendotheliosis virus, subtype 2, was isolated from samples of liver and spleen.

Animals↗
PubMed1988

Disseminated sarcocystosis in a cat with lymphosarcoma.

Cysts of the protozoan Sarcocystis sp were found in skeletal and cardiac musculature in a 1.5-year-old cat with lymphosarcoma. The cat was FeLV-positive and had grossly visible neoplastic involvement of the spinal cord, mediastinum, bone marrow, and kidneys. Ultrastructural examination of the parasitic cyst wall suggested that the species in this case was different from that described in the only other reported case. It was hypothesized that immunosuppression from FeLV infection permitted an aberrant life cycle with encystment of Sarcocystis sp in this cat.

Animals↗
PubMed1984

Acute monensin toxicosis in sheep: light and electron microscopic changes.

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.

Acute Disease↗
PubMedDate not supplied

Breeder turkey hens seropositive and culture-negative for Mycoplasma synoviae.

Four flocks of clinically normal turkey breeder hens were shown to have suspect and positive Mycoplasma synoviae (MS) hemagglutination-inhibition (HI), enzyme-linked immunosorbent assay, and, in some cases, serum plate agglutination serology in the absence of MS isolation. In all cases, HI serology for Mycoplasma gallisepticum (MG) and M. meleagridis was negative. Acholeplasma laidlawii was isolated from some hens in each of these MS-seropositive culture-negative flocks. Immunoblotting was used to help determine if this positive MS serology was a result of cross-reactive antibodies to A. laidlawii or to some other Mycoplasma species. When sera from two of the flocks were reacted with MS antigen in immunoblotting, a strong and characteristic MS immunoblot profile was seen. Immunoblotting gave no evidence of a strong antibody response to A. laidlawii, M. iowae, or MG. This suggests the presence (or earlier presence) of MS in these flocks that is difficult to isolate by routine methods. Furthermore, this work shows that immunoblotting can be an important tool in the diagnosis of poultry diseases.

Acholeplasma laidlawii↗
PubMedDate not supplied

Vaccination of turkeys with cell-free culture filtrate of Pasteurella multocida: effects of dilution, iron chelation, and heterologous challenge.

Two experiments were done to further define cell-free culture filtrate (CCF) from Pasteurella multocida and its endotoxin content in protecting turkeys against challenge. In the first experiment, the greater-than-30,000-molecular-weight fraction of P. multocida strain R44/6 (serotype 3/4/9/12) CCF was used in 10-fold dilutions given by air-sac inoculation or aerosol to vaccinate turkeys, which were subsequently challenged with either homologous (P-1059, serotype 3) or heterologous (X-73, serotype 1) strains. Endotoxin content of the CCF fraction was high. Compared with positive controls given either live Clemson University vaccine or a commercial bacterin, homologous protection was provided by undiluted CCF and 1:10 dilutions of CCF, but there was no heterologous protection. In the second experiment, CCF of strain R44/6 in regular and iron-limiting media and CCF of strain FC127B (serotype 1/4) were used alone or in combination to vaccinate turkeys, which were challenged as in the first experiment. Homologous but not heterologous protection occurred, even though growth of strain R44/6 in iron-limiting media reduced endotoxin content of CCF by approximately 93%. These results indicate that endotoxin levels of less than 10% but greater than 1% of those in CCF from regular media are sufficient to induce protection in turkeys against homologous challenge but that CCF from either regular or iron-limiting medium does not provide protection against heterologous challenge.

Aerosols↗
PubMedDate not supplied

Vaccination of turkeys with cell-free culture filtrate of Pasteurella multocida: effects of ultrafiltration and endotoxin removal.

Cell-free culture filtrate (CCF) of Pasteurella multocida strain R44/6 (serotype 3/4/9/12) was fractionated by ultrafiltration into fractions of less than 10,000, greater than 10,000, greater than 30,000, and 10,000 to 30,000 molecular weight (MW). The less-than-10,000-MW fraction contained little endotoxin comparable to bacteriologic medium; the 10,000-to-30,000-MW fraction had a moderate amount of endotoxin, whereas the greater-than-10,000- and greater-than-30,000-MW fractions contained high levels of endotoxin. Following ultrafiltration, each fraction, except the less-than-10,000-MW fraction, was divided into two equal parts, and endotoxin was removed from one part. Turkeys were vaccinated with the various MW fractions of CCF, with and without endotoxin, via the air sacs at 6 and 9 weeks of age and compared with negative controls given bacteriologic medium and positive controls vaccinated with a commercial bacterin. Before oral challenge with strain P-1059 (serotype 3) at 12 weeks of age, antibody titers were detected only in positive control turkeys. Protection against challenge, as measured by post-challenge mortality and body-weight gain, was provided by the greater-than-10,000-, greater-than-30,000-, and 10,000-to-30,000-MW fractions containing endotoxin and the commercial bacterin. Turkeys that had been vaccinated with bacteriologic medium and the four different fractions without endotoxin were not protected. Results indicated that endotoxin in CCF of P. multocida is critical in protecting turkeys from pasteurellosis.

Air Sacs↗
PubMedDate not supplied

Vaccination of turkeys with cell-free culture filtrate of Pasteurella multocida.

Turkeys given cell-free culture filtrate (CCF) of Pasteurella multocida strain R44/6 orally, via air sacs, or subcutaneously mixed 1:1 with incomplete Freund's adjuvant (IFA) at 6 and 9.5 weeks of age were compared with negative controls given bacteriologic medium and positive controls vaccinated with a commercial bacterin. At 13 weeks of age, serum antibody titers to P. multocida were detectable only in turkeys given CCF in IFA (low titers) and positive control turkeys (high titers), at which time turkeys were challenged orally with either the homologous strain or strain P-1059. Protection against challenge with strain R44/6 was provided by the commercial bacterin, CCF in IFA, and CCF given via air sacs. When turkeys were challenged with strain P-1059, protection was superior in turkeys given CCF via air sacs, intermediate in turkeys given commercial bacterin or CCF in IFA, and absent in negative control turkeys and turkeys given CCF orally. These results indicate CCF is an effective immunogen when administered via the lower respiratory tract for protecting turkeys against pasteurellosis.

Administration, Oral↗
PubMedDate not supplied

Blood clearance of radiolabeled gold colloid by the turkey mononuclear phagocytic system.

Radiolabeled gold colloid (198Au), which has been used to assess particle clearance in mammalian species, was used to assess blood-borne particle clearance in turkeys. When turkeys 16 weeks of age were injected intravenously with these particles, there was greater than a 98% decrease in blood gamma emission from 1 minute to 6 minutes postinjection. Uptake of particles was predominantly hepatic with minor uptake by the spleen and bone marrow. Negligible uptake was observed in lung, kidney, and skeletal muscle. Autoradiography demonstrated particles within Kupffer cells of the liver, periarteriolar macrophages of the spleen, and bone-marrow macrophages. Particles could not be demonstrated within the lung or kidney. The mononuclear phagocyte system responsible for blood particle clearance in turkeys is therefore located predominantly within the liver, spleen, and bone marrow and is similar to that of rats, mice, rabbits, and dogs. Pulmonary intravascular macrophages, which have recently been described in ruminants and pigs, are not apparent in this species.

Animals↗
PubMedDate not supplied

An outbreak of influenza (H1N1) in turkey breeder hens.

Outbreaks of influenza were diagnosed in two turkey breeder flocks on the same premises in eastern North Carolina during the "dark-out" period of recycling for a second lay. Clinical history included increased mortality from acute death with no apparent predisposing illness. Mortality attributed to the disease was 4.5% in one flock and 3.3% in the other. Necropsy findings included severe diffuse congestion and edema of both lungs, with little or no pleural exudate. Spleens were moderately to markedly enlarged and mottled, and kidneys were swollen and congested. Microscopic lesions included moderate to severe serofibrinous pneumonia with severe pulmonary congestion. Splenic changes included fibrin deposition and severe congestion, and severe congestion was noted in kidneys. Influenza virus (H1N1) was isolated from pools of tissues including lung, spleen, liver, and kidney, and both flocks seroconverted to influenza (H1N1) virus.

Animals↗
PubMedDate not supplied

Monensin toxicity in turkey breeder hens.

High mortality in two flocks of 1900 turkey breeder hens accidentally fed 280 g monensin/ton of complete feed is described. Mortality attributed to the poisoning was 76% in flock 1 and 18% in flock 2. Clinically, turkeys were found dead, exhibited respiratory distress with wings extended laterally, had fine tremors, or showed posterior paresis and inability to rise. The most striking finding at necropsy was the almost complete absence of gross lesions. Some turkeys had severely congested lungs; however, many did not. A few birds had pale streaks within the adductor muscles of the legs. Microscopic lesions included myofiber degeneration and necrosis of skeletal and myocardial muscle. Serum phosphorus, lactate dehydrogenase, and creatine phosphokinase were markedly elevated, whereas potassium, chloride, and calcium values were lowered.

Animal Feed↗
PubMedDate not supplied

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↗