Inhibition of feline infectious peritonitis virus replication by recombinant human leukocyte (alpha) interferon and feline fibroblastic (beta) interferon

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extracellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.     

Etiology of ammoniated hay toxicosis

Some animals consuming hay treated with anhydrous ammonia have developed neurological signs including hyperexcitability, circling and convulsions. A series of experiments was conducted to identify tentatively the toxin and determine its mode of action. Three out of four sheep fed ammoniated orchardgrass hay (approximately 4% ammonia on a dry basis) developed convulsions. Two of the three sheep died within 18 h of the onset of signs. The concentrations of blood lactate and pyruvate were elevated in the symptomatic sheep (P less than .05). A proposed toxin, 4-methyl imidazole, did not induce the syndrome when 750 mg/d (approximately 10 times the dietary amount) were administered orally. Four out of five calves that received milk from cows fed ammoniated oat hay (approximately 5% ammonia on dry basis) displayed hyperexcitability and circling. Concentrations of blood lactate and pyruvate were also elevated in the calves. The crude alkaloid fraction of the toxic milk produced neurological signs similar to those of the calves when injected into mice. A fluorescent compound was found in the alkaloid fraction of toxic milk and ammoniated hay, but not in control milk or untreated hay. The fluorescent compound was quite labile; hence, characterization has been unsuccessful thus far.     

RADIOGRAPHIC CHANGES IN TESTES OF BULLS INFECTED WITH BESNOITIOSIS

Ten beef bulls infected with Besnoitiosis were examined radiographically and pathologically. Eight of these were slaughtered soon after diagnosis; two were left for a six-month observation period. The radiographic findings were focal and branching-tree calcification of the testes. Histopathologic examination proved these calcifications to be necrotic sections of the seminiferous tubules. Radiography of the testes as a means of evaluating the fertility status of the infected bull is recommended.     

Recognition and classification of dysmyelopoiesis in the dog: a review

Dysmyelopoiesis is defined as a hematologic disorder characterized by the presence of cytopenias in the blood and dysplastic cells in one or more hematologic cell lines in the blood or bone marrow. The causes of dysmyelopoiesis include acquired mutations in hematopoietic stem cells (i.e., myelodysplastic syndromes [MDSs]), congenital defects in hematopoiesis, and dysmyelopoietic conditions associated with various disease processes, drug treatments, or toxin exposure. Two major subtypes of MDSs (i.e., MDS with refractory cytopenias and MDS with excess myeloblasts) have been described that differ in clinical presentation, response to treatment, and survival time. The most frequently occurring causes of secondary dysmyelopoiesis include immune-mediated hematologic diseases, lymphoid malignancies, and exposure to chemotherapeutic drugs. Differentiation of the various causes of dysmyelopoiesis is essential for establishing an appropriate therapeutic plan and for determining prognosis.