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Biomedical subjects

C E Greene

Publications and source records attributed to C E Greene.

69 records · Page 4Linked to original sources

Coagulation properties of fresh-frozin canine plasma during prolonged storage.

Coagulation properties of fresh platelet-poor canine plasma from 20 dogs were examined before freezing and after storage at intervals of up to 1 year. Prothrombin time and factor V activity did not change in frozen plasma when compared with data obtained after plasma was stored 1 week. When compared with that of fresh plasma, activated partial thromboplastin time shortened and factor VIII activity decreased after freezing and thawing of fresh plasma after 1 week, activated partial thromboplastin time in fresh-frozen plasma gradually shortened during the year of storage. Factor viii activity increased in the first 4 months of storage, but gradually decreased by 1 year.

Animals↗

Myopathy associated with hyperadrenocorticism in the dog.

Naturally occurring or iatrogenic hyperadrenocorticism was associated with myopathy in six dogs. One dog had muscle weakness and muscle atrophy but normal electromyographic findings. Five dogs had muscle stiffness, proximal appendicular muscle enlargement, and myotonic discharges on electromyography. Histologic, electron microscopic, and histochemical findings in the musculature of dogs that were examined were characteristic of noninflammatory degenerative myopathy. Clinical signs of the myopathy improved to varying degrees in five dogs that were treated for the hyperadrenocorticism.

Animals↗

Congenital cerebrospinal hypomyelinogenesis in a pup.

One of 8 highly inbred Dalmatian pups was born with generalized body tremors, which interfered with the pup's ability to suckle, walk, and maintain sternal recumbency. The pup's head, neck, and limbs oscillated rhythmically when it attempted to perform any motor function. The pup was euthanatized at 8 weeks of age, after it became apparent that the disorder was likely to be permanent. The histologic diagnosis was cerebrospinal hypomyelinogenesis.

Animals↗

Cold hemagglutinin disease in a dog.

Cold hemagglutinin disease, a form of autoimmune hemolytic anemia caused by cold-acting erythrocyte autoantibodies, was diagnosed in a dog. Cold-acting antibodies differ from warm-acting antibodies in several ways, including temperature-dependent reactivity below 32 C. The autoantibody in this case (immunoglobulin M) was in the serum in higher than normal concentrations and was reactive at temperatures approaching freezing. The course of the disease was chronic and was characterized by cyanosis and necrosis of the body extremities. Immunosuppressive therapy with corticosteroids was successful in alleviating the clinical signs and reducing the autoantibody activity in the dog. The cause of this disorder was not determined.

Agglutinins↗

Disseminated intravascular coagulation complicating aflatoxicosis in dogs.

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.

Aflatoxins↗

Lissencephaly in two Lhasa Apso dogs.

Lissencephaly, a congenital absence of cerebrocortical convolutions, was discovered in 2 Lhasa Apso dogs by clinical and pathologic evaluation. Neurologic abnormalities, which became evident within the 1st year of life, included behavioral, visual, and convulsive disorders. The neurologic abnormalities were mild or delayed in onset after birth, indicating the dog is less dependent on the cerebral cortex for sensorimotor function than is man.

Animals↗

Neoplasms of mesenchymal origin in the spinal cord and nerve roots of three dogs.

Clinicopathological findings of three different neoplastic conditions involving the spinal cord and nerve roots in three dogs are described. One sarcomatous intra-medullary tumor closely associated with the vasculature was classified as a reticulum cell sarcoma of the spinal cord. The second case had massive and widespread neoplastic proliferation of reticulohistiocytic cells around the perineurinal vessels of many spinal nerve roots. The process was classified as a primary neoplastic reticulosis of the spinal roots. Multiple highly malignant tumors, infiltrating the spinal cord were found in one thoracic and several lumbosacral spinal nerve roots in the third case. These were considered to be anaplastic neurofibrosarcomas because of high collagen content, intact nerve fibers, whorl formation, and the tendency to palisade in some areas.

Animals↗

Lower motor neuron disease with accumulation of neurofilaments in a cat.

A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.

Animals↗

Fibrocartilaginous emboli as the cause of ischemic myelopathy in a dog.

Acute hemiplegia and Horner's syndrome developed in a 6-year-old female black Labrador Retriever 24 hours after a day of exercise. Radiographic, cerebrospinal fluid, and electromyographic studies did not detect the site or nature of the suspected cervical lesion. The dog showed no improvement after evaluation for 5 days on corticosteroid and antibiotic therapy. Gross and microscopic examination revealed the presence of an ischemic infarct in the C6 segment of the cervical spinal cord and associated fibrocartilaginous emboli. The nature of the clinical signs and the pathologic findings in this case are similar to previous reports of human and canine cases.

Animals↗

Clinical feline toxoplasmosis. Serologic diagnosis and therapeutic management of 15 cases.

Clinical toxoplasmosis was diagnosed in 15 cats by correlating serologic evidence of infection and clinical signs to either response to therapy or histopathologic demonstration of the organism. Ophthalmic manifestations, primarily involving the anterior segment, were common. Other common physical examination abnormalities included muscle hyperesthesia, fever, and weight loss. Response to therapy was variable, but administration of clindamycin hydrochloride resulted in resolution of all clinical signs not involving the eyes in surviving animals. This drug, alone or in combination with corticosteroids, led to total resolution of clinical signs in four of four cats with active retinochoroiditis and in six of nine cats with anterior uveitis. Four of the 15 cats had concurrent infection with feline immunodeficiency virus (FIV). Feline leukemia virus antigen or antibodies to feline infectious peritonitis virus were not detected.

Animals↗

Effect of feline immunodeficiency virus infection on Toxoplasma gondii-specific humoral and cell-mediated immune responses of cats with serologic evidence of toxoplasmosis.

Serum samples from 89 cats with serologic evidence of toxoplasmosis were identified by using an enzyme-linked immunosorbent assay (ELISA) that detected Toxoplasma gondii-specific immunoglobulin M (IgM) or T. gondii-specific immunoglobulin G (IgG). Concurrent feline immunodeficiency virus (FIV) infection was detected in 36 cats using an ELISA for detection of FIV-specific IgG. The majority of the cats in both the FIV-seropositive and FIV-seronegative groups were male and > 5 years of age. FIV-seropositive cats were more likely to have T. gondii IgM titers without IgG (P < 0.05) or any T. gondii IgM titer (P < 0.05) than were FIV-seronegative cats. FIV-seronegative cats (1328) had a higher T. gondii IgG geometric mean titer than did FIV-seropositive cats (724) and were more likely to have T. gondii IgG titers > 1:2048 than were FIV-seropositive cats (P < 0.05). Cats with serologic evidence of both T. gondii and FIV infections had persistent T. gondii IgM titers for > 12 weeks. Lymphoblast transformation in response to concanavalin A, T. gondii-specific intracellular antigens, and T. gondii-specific secretory antigens was compared in T. gondii seropositive and FIV-seronegative cats, cats with serologic evidence of T. gondii infection alone, and cats with serologic evidence of concurrent FIV and T. gondii infections. Lymphocytes from all but one cat in the FIV-seropositive group responded to concanavalin A. Whereas lymphocytes from FIV-seronegative cats with serologic evidence of toxoplasmosis responded to T. gondii-specific antigens, four of five of the FIV-seropositive cats with concurrent serologic evidence of toxoplasmosis did not.

Animals↗

Relationship of lower urinary tract signs to seropositivity for feline immunodeficiency virus in cats.

A group of 41 cats with signs of lower urinary tract disease was compared to a group of 41 cats without any history of disease for prevalence of seropositivity for feline immunodeficiency virus (FIV). The group of healthy cats was similar in age and gender to the group of cats with signs of lower urinary tract disease. Three of the cats with lower urinary tract disease and one control cat were seropositive for FIV. This difference was not statistically significant. The most common cause of lower urinary tract signs was idiopathic. Only 7 cats had urinary tract infection, most associated with perineal urethrostomy or catheterization. Six of the cats with bacterial urinary tract infections were FIV negative.

Animals↗

Disseminated Mycobacterium avium--intracellulare complex infection in a miniature schnauzer.

A two-year-old, spayed female, miniature schnauzer was evaluated for respiratory distress associated with a compressive cervical mass. Generalized mycobacterial infection was diagnosed from aspirates of several enlarged lymph nodes. Tissue specimens further identified Mycobacterium avium--intracellulare using polymerase chain reaction followed by nucleic acid hybridization. Treatment with enrofloxacin, clofazamine, rifampin, and interferon did not result in long-term success.

Animals↗