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Biomedical subjects

C E Greene

Publications and source records attributed to C E Greene.

At least 37 records · Page 2Linked to original sources
PubMed1992

Ehrlichia ewingii sp. nov., the etiologic agent of canine granulocytic ehrlichiosis.

The 16S rRNA gene was amplified, cloned, and sequenced from the blood of two dogs that were experimentally infected with the etiologic agent of canine granulocytic ehrlichiosis. The 16S rRNA sequence was found to be unique when it was compared with the sequences of other members of the genus Ehrlichia. The most closely related species were Ehrlichia canis (98.0% related) and the human ehrlichiosis agent (Ehrlichia chaffeensis) (98.1% related); all other species in the genus were found to be phylogenetically much more distant. Our results, coupled with previous serologic data, provide conclusive evidence that the canine granulocytic ehrlichiosis agent is a new species of the genus Ehrlichia that is related to, but is distinct from, E. canis and all other members of the genus. We propose the name Ehrlichia ewingii sp. nov.; the Stillwater strain is the type strain.

Animals↗
PubMed1991

Factor XII and partial prekallikrein deficiencies in a dog with recurrent gastrointestinal hemorrhage.

Factor XII deficiency and impaired prekallikrein activity were diagnosed in a 1-year-old Chinese Shar Pei. The dog experienced repeated episodes of intestinal hemorrhage and diarrhea. Laboratory findings were compatible with blood loss (iron deficiency anemia and hypoproteinemia). Necropsy findings suggested mild infiltrative bowel disease that could have been responsible for the dog's diarrhea, but no explanation for the severe recurrent gastrointestinal hemorrhage could be found. Factor XII deficiency is uncommon in the dog and is not associated with hemorrhagic tendencies. The factor XII deficiency in this case may have contributed to the gastrointestinal hemorrhage.

Animals↗
PubMed1990

Intestinal malabsorption and cryptosporidiosis in an adult dog.

Chronic intestinal cryptosporidiosis was diagnosed as the cause of chronic diarrhea and weight loss in an adult dog without obvious signs of immunosuppression. Results of tests for digestive function suggested that the dog had impaired intestinal absorption or bacterial overgrowth. The nutrient malabsorption might have resulted in or have been caused by the cryptosporidiosis. Temporary clinical improvement without reduction in fecal oocyst concentration was noticed following treatment with clindamycin. The dog was euthanatized. At necropsy, the dog was found to have chronic lymphoplasmacytic enteritis and cryptosporidiosis. A veterinary student that worked in the ward where the dog was kept developed cryptosporidal diarrhea.

Animals↗
PubMed1990

Evaluation of ketoconazole and itraconazole for treatment of disseminated cryptococcosis in cats.

During the first part of a study, cats were inoculated with Cryptococcus neoformans via the following routes: intradermal, intranasal, IV, and intracisternal. Only use of the IV route of inoculation consistently induced disseminated cryptococcosis. In the second part of the study, disseminated cryptococcosis was experimentally induced in cats via IV inoculation of C neoformans. One month after inoculation, 3 cats were treated with ketoconazole (10 mg/kg of body weight/d) and 3 cats were treated with itraconazole (10 mg/kg/d) for 3 months. One of the ketoconazole-treated and 2 of the itraconazole-treated cats also had cryptococcosis of the CNS when treatment was begun. During treatment, serum cryptococcal antigen titer progressively decreased in all cats. Abnormalities in CBC values or the serum biochemical profile were not found in any cat during treatment. However, all ketoconazole-treated cats became anorectic and lost weight. Side effects were not seen in itraconazole-treated cats. During the 3-month posttreatment observation period, all cats remained healthy. At necropsy, histologic evidence of cryptococcosis was not found in the 3 ketoconazole-treated cats or in 2 of the itraconazole-treated cats. In the third itraconazole-treated cat, cryptococcal organisms were found in the kidneys.

Animals↗
PubMed1989

Prevalence of Toxoplasma gondii infection in cats in Georgia using enzyme-linked immunosorbent assays for IgM, IgG, and antigens.

Serologic prevalence of Toxoplasma gondii infection was determined using enzyme-linked immunosorbent assays detecting immunoglobulin M (IgM), immunoglobulin G (IgG), and circulating T. gondii antigens (Ag) in 81 healthy cats and 107 cats with clinical signs referable to toxoplasmosis. A higher prevalence of infection was detected using the three assays together in healthy cats, clinically ill cats, and combined healthy and clinically ill cats than when IgG class antibody detection alone was used. IgM titers greater than or equal to 1:256 and IgG titers greater than or equal to 1:512 were present more frequently in cats with clinical signs of disease. Prevalence of present or prior infection as defined by these three assays combined increased with advancing age in both groups of cats.

Animals↗
PubMed1989

Experimental visceral leishmaniasis in the opossum.

Adult wild-trapped opossums were infected with Leishmania donovani (Khartoum strain, WR 378) and evaluated as an animal model of visceral leishmaniasis. All infected opossums died within 32 days. Loss of body fat, hepatomegaly, and petechiae of skin and abdominal musculature were seen at necropsy. Microscopically, numerous amastigote-laden macrophages were seen in histologic sections of liver, spleen, and lymph nodes; fewer parasite-laden macrophages were in the bronchial-associated lymphoid tissues and renal glomeruli. Hematological findings included thrombocytopenia (terminal), neutropenia, and lymphopenia. Blood lymphocyte blastogenesis in response to concanavalin A and phytohemagglutinin was decreased markedly at day 24 post-infection (PI). Serum antibodies (1:40 dilution) to promastigotes of L. donovani were detected in five of eight infected opossums tested on days 10 and 24 PI. Total bilirubin concentrations and alanine aminotransferase and aspartate aminotransferase activities were increased after day 25 PI. Activated partial thromboplastin times and one-stage prothrombin times were prolonged before death. Concurrently, factors V, VIII, and XII activities were decreased.

Animals↗
PubMed1989

Diagnosis of recent Toxoplasma gondii infection in cats by use of an enzyme-linked immunosorbent assay for immunoglobulin M.

Subclinical Toxoplasma gondii infection was induced in young and adult cats by oral administration of tissue cysts. An antibody-capture ELISA to detect anti-Toxoplasma IgM-class antibodies in the serum of cats was developed. The serologic response to experimental infection was followed in the 2 groups of cats by use of anti-Toxoplasma IgM and IgG detection. This study shows that anti-Toxoplasma IgM-class antibody titers develop early in the course of experimental infection in cats and that the combination of IgM- and IgG-class antibody titer measurement can aid in the detection of recent subclinical toxoplasmosis.

Animals↗
PubMed1989

Enzyme-linked immunosorbent assay for the detection of circulating antigens of Toxoplasma gondii in the serum of cats.

An ELISA was developed to detect circulating antigens of Toxoplasma gondii in the serum of cats. For the experiment, toxoplasmosis was induced in a group of cats by oral administration of bradyzoites. An ELISA that detects anti-Toxoplasma IgG, an ELISA to detect circulating antigens, and fecal examinations were performed on samples from each cat for 1 year after inoculation. When coupled with IgG-class antibody measurement, antigen detection can aid in the diagnosis of some cases of subclinical feline toxoplasmosis.

Animals↗
PubMed1989

Effect of clindamycin on factor-VII activity in healthy cats.

Four healthy cats were given clindamycin orally in daily doses of 25 or 50 mg/kg of body weight for 6 weeks. Significant change in Factor-VII activity was not found, compared with pretreatment values. In 2 cats tested, toxin produced by Clostridium difficile was not detected in fecal samples obtained before treatment and at 6 weeks after treatment, suggesting that intestinal overgrowth by C difficile did not develop. Results of the study seemed to indicate that orally administered clindamycin does not measurably reduce synthesis of vitamin K-dependent clotting factors in healthy cats.

Animals↗
PubMed1988

Surgical management of bilateral diaphragmatic paralysis in a dog.

Bilateral diaphragmatic paralysis of uncertain cause developed in a 3-month-old Golden Retriever. A surgical procedure for tightening the diaphragmatic muscle was used to help alleviate the dog's respiratory distress. During thoracotomy, the central tendon of the diaphragm was plicated, using an interlocking suture pattern. The dog improved after surgery, and although complete recovery from paralysis was achieved only on one side, the dog has remained clinically normal 1 year after surgery.

Animals↗
PubMed1988

Experimentally induced bluetongue virus infection in white-tailed deer: coagulation, clinical pathologic, and gross pathologic changes.

Ten yearling white-tailed deer (Odocoileus virginianus) were inoculated with bluetongue virus serotype 17. Two yearling white-tailed deer were inoculated with sonicated heparinized noninfected blood and served as controls. Clinical signs of bluetongue virus infection included increased rectal temperature, erythema, facial edema, coronitis, and stomatitis. By postinoculation day (PID) 8, excessive bleeding and hematoma formation at venipuncture sites, dehydration, and diarrhea developed. At necropsy, the most consistent findings were oral lesions and widespread hemorrhage, which ranged from petechia to massive hematoma formation. Bluetongue virus caused progressive prolongation of activated partial thromboplastin time and prothrombin time, and progressive reduction of Factors VIII and XII plasma activities beginning on PID 6. A progressive decrease in platelet numbers also developed on PID 6. Changes in platelet size were not detected. Mean thrombin time was shortened, but prolongation developed in 1 deer. Mean fibrinogen concentration and Factor V plasma activity initially increased and then decreased, but remained above preinoculation values. Factor V activity was low in a few deer. Results of screening tests for inhibitors of the intrinsic coagulation system were positive in 2 deer. High concentrations of fibrin(ogen) degradation products were first detected between PID 3 and 6. Hematologic changes included leukopenia, lymphopenia, neutrophilia, and low total plasma protein concentration. Differences in PCV, hemoglobin concentration, or RBC counts were not detected between infected and control deer. Serum total bilirubin concentration increased by PID 6, primarily because of increased unconjugated bilirubin concentration. Mild to severe increases in serum aspartate transaminase activity were accompanied by more marked increases in creatine kinase activity. Indirect Coombs test results were negative in all deer.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Induced aflatoxicosis in rabbits: blood coagulation defects.

The effect of acute and subchronic experimental aflatoxicosis on blood clotting activity and platelets was evaluated. Male New Zealand White rabbits (weighing 2.4-3.2 kg each) were used. In Experiment 1, 19 rabbits were given orally 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily from Day 0 through Day 23. Blood samples were collected before dosing and on Days 2, 5, 9, 12, 16, 19, and 23 of the experimental period. In Experiment 2, 40 rabbits were given a single dose of 0.4 mg of AFB1/kg of body weight. Blood samples were collected before dosing and at 12, 24, 36, and 48 hr after dosing. When compared to baseline and control animal values, one-stage prothrombin times and activated partial thromboplastin times of aflatoxin-dosed rabbits were lengthened, and there was a statistically significant decrease in fibrinogen, Factor IX, VIII, and V activities. Platelet counts were significantly increased in subacutely exposed rabbits, and platelet size was decreased in single high-dose treated groups. Factor deficiencies were attributed to a combination of decreased factor synthesis from hepatic insufficiency and consumptive coagulopathy or primary fibrinolysis.

Administration, Oral↗
PubMed1986

Antidotal effect of vitamin K1 against warfarin-induced anticoagulation in horses.

Warfarin-induced anticoagulation and reversal of the induced anticoagulation by vitamin K1 were evaluated in 4 mature horses. Each horse was given warfarin IV until the prothrombin (PT) time was prolonged by approximately 1.5 times the predosing base-line value. In experiment 1, we evaluated the time required for PT to return to the predosing value (PT reversal time) after warfarin administration was discontinued. Between each experiment, a 1-week rest period was allowed. In experiment 2, two doses of vitamin K1 (100 mg/dose) were administered IM 6 hours apart, and the PT was monitored hourly for 24 hours. In experiments 3 and 4, the horses were dosed with warfarin as in experiment 1, and the PT reversal time was evaluated after administration of 300- and 500-mg doses of vitamin K1 IM, respectively. In experiment 5, one horse was eliminated from the study, 1 horse was given 300 mg of vitamin K1 IV, and 2 horses were given 300 mg of vitamin K1 subcutaneously (SC); the reversal times were evaluated in the 3 horses given vitamin K1. Therapeutic response time was designated as the time required for the mean PT time of treated horses to reach the midpoint between the longest mean PT time achieved during anticoagulation and the mean base-line PT time. The therapeutic response time, without supportive therapy, after discontinuation of warfarin administration was 30 hours, and there was a PT reversal time of approximately 5 days from the last dose of warfarin. The 100-mg dose of vitamin K1 shortened the therapeutic response time to 12 hours and the PT reversal time to 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Coagulation abnormalities associated with acute Angiostrongylus vasorum infection in dogs.

Ten dogs were experimentally infected with 150 3rd-stage larvae of the lungworm Angiostrongylus vasorum (Baillet, 1866). Blood samples obtained once a week for 5 weeks after infection was induced were examined for coagulation alterations. Thrombocytopenia developed in infected dogs before and after parasitic patency, which occurred 6 weeks after infection was induced. Prolongation of activated partial thromboplastin time and thrombocytopenia initially were associated with periods of larval migration and, later, at patency, with pulmonary egg embolism and hatching of 1st-stage larvae in the lung. Decreased factor-V activity, significantly shortened values for the prothrombin time, and increased factor-VIII activity were evident during postpatent periods of parasitic infection. Significant changes were not found in factors-XII and -IX activities throughout the course of infection. Coagulation abnormalities were attributed to excessive intravascular coagulation. Immature adults and first stages of the parasite seemed to have initiated the coagulopathy in the prepatent phase of infection, with subsequent coagulation abnormalities occurring at the time of patency.

Acute Disease↗
PubMed1985

Trichosporon infection in a cat.

A protruding nasal mass in a domestic shorthair cat with nasal discharge and recurrent fever was determined to be caused by infection with the fungus Trichosporon pullulans, as determined by cytologic, histologic, and fungal culture methods. Initially, the cat was treated orally with ketoconazole and the mass decreased in size. When signs of hepatotoxicosis developed, treatment was reduced to an alternate-day basis. However, the nasal mass increased in size with this regimen, and therapy with amphotericin B and 5-flucytosine was begun. It also was unsuccessful.

Amphotericin B↗