Polioencephalomalacia (PEM) is a neuropathologic condition of ruminants that can be induced by a variety of neural metabolic disruptions. These include altered thiamine status, water deprivation-sodium ion toxicosis, lead poisoning, and high sulfur intake. Investigations of sulfur-related PEM have demonstrated that the onset of the clinical signs coincides with excessive ruminal sulfide production. A number of ruminal factors could modulate the production and absorption of ruminal sulfide. The development of a convenient method to estimate ruminal gas cap H2S has made it possible to identify cattle with high levels of ruminal H2S and evaluate their risk of developing PEM.

ABSTRACT:We studied the effects of natural and/or experimental infections of West Nile virus (WNV) in five raptor species from July 2002 to March 2004, including American kestrels (Falco sparverius), golden eagles (Aquila chrysaetos), red-tailed hawks (Buteo jamaicensis), barn owls (Tyto alba), and great horned owls (Bubo virginianus). Birds were infected per mosquito bite, per os, or percutaneously by needle. Many experimentally infected birds developed mosquito-infectious levels of viremia (.10 5 WNV plaque forming units per ml serum) within 5 days postinoculation (DPI), and/ or shed virus per os or per cloaca. Infection of organs 15-27 days postinoculation was infrequently detected by virus isolation from spleen, kidney, skin, heart, brain, and eye in convalescent birds. Histopathologic findings varied among species and by method of infection. The most common histopathologic lesions were subacute myocarditis and encephalitis. Several birds had a more acute, severe disease condition represented by arteritis and associated with tissue degeneration and necrosis. This study demonstrates that raptor species vary in their response to WNV infection and that several modes of exposure (e.g., oral) may result in infection. Wildlife managers should recognize that, although many WNV infections are sublethal to raptors, subacute lesions could potentially reduce viability of populations. We recommend that raptor handlers consider raptors as a potential source of WNV contamination due to oral and cloacal shedding.

The clinical signs and morphological brain lesions associated with histotoxic hypoxia induced by subcutaneous injection of 3-nitropropionic acid (NPA) in rats are described, and compared to hypoxic brain damage from other causes including ischemia and hypoglycemia. The brains were perfusion-fixed with paraformaldehyde/glutaraldehyde fixative, and examined by light and electron microscopy. Intoxicated rats developed severe neurological disease characterized by somnolence, uncoordinated gait with stereotypical paddling movements, and ventral or lateral recumbency. Recumbent rats had a selective, bilaterally symmetrical pattern of severe morphological injury in the caudate-putamen, hippocampus, and thalamus. Recumbency was a consistent indicator of the development of morphological brain lesions. In contrast to reports describing rat models of ischemia and hypoglycemia, morphological injury was not seen in the cerebral and cerebellar cortices of NPA-intoxicated rats. Ultrastructurally, neuronal alterations ranged from chromatin clumping with increased cytoplasmic lucency to severe cellular shrinkage or swelling with marked mitochondrial swelling (high amplitude swelling). White matter alterations included axonal swelling and adaxonal splitting of myelin lamellae. Vascular changes included perivascular deposits of proteinaceous material presumably from leakage of serum proteins, variable electron lucency of endothelial cell cytoplasm, an apparent increase in pinocytotic vesicles, rare platelet thrombosis of capillaries, and rare intravascular blebs of luminal plasma membrane. As a model of brain damage following energy deficiency, NPA intoxication has the advantages of producing morphological brain injury in a highly predictable anatomical pattern, and at a time paralleling the onset of clinical recumbency.

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Abstract. Two groups of 3 120-160-kg Holstein steers were fed a diet high in carbohydrate and low in long fiber and either with or without added sodium sulfate. Prior to and during the course of feeding the experimental diet, the concentrations of rumen hydrogen sulfide gas and rumen fluid sulfide were determined by a simple sulfide detector tube method and by sulfide-selective electrode, respectively. Other measurements included rumen fluid pH, blood creatine kinase, and blood sulfhemoglobin. Two of the 3 steers fed the high-sulfate diet developed signs and lesions of polioencephalomalacia. Clinical signs included episodic ataxia and blunted or absent menace reaction. Increased ruminal H 2 S gas concentrations occurred in all 3 steers consuming the diet with added sulfate. The onset of clinical signs coincided with the onset of elevated H 2 S concentrations. These increases were 40-60 times the values measured in the steers consuming the diet without added sulfate. In contrast, increases in rumen fluid sulfide concentrations usually rose to 4 times that of control steers. The steers fed an identical diet but without added sulfate exhibited no signs or lesions of polioencephalomalacia and no elevations of sulfide in rumen gas or fluid. All steers had a modest decrease in rumen fluid pH associated with the transition to the concentrate diet. No significant changes were observed in any of the blood measurements of any of the steers. An additional pair of steers was fed the experimental diet with or without added sulfate to compare the ruminal H 2 S gas concentrations estimated by H 2 S detector tubes with those estimated by a different method of analysis utilizing charcoal trapping of H 2 S, conversion to sulfate, and measurement of the sulfate. Both methods yielded comparable estimates of H 2 S concentration. Overall, these data indicate that changes in rumen gas cap H 2 S concentrations are larger than changes in rumen fluid sulfide concentration and that estimation of rumen gas cap H 2 S concentration may be a practical approach to detecting pathologic increases in ruminal H 2 S gas. This simple, rapid, minimally invasive method should be useful for estimating the H 2 S content of ruminal gas under field conditions. Polioencephalomalacia 15 (PEM) is one of the most the induced PEM, 10 but it was not possible to demcommon neuropathologic alterations of cattle 15,27 and onstrate alterations in thiamine status in steers conis associated with several types of metabolic or toxic suming the experimental diet. 10,25 PEM was caused by alterations, including thiamine deficiency, 13 acute lead sulfide directly, not by some other product of disturbed poisoning, 4 and sometimes sodium toxicosis/water de-ruminal metabolism, as was demonstrated by the inprivation. 23 Another form of PEM that is being in-duction of PEM in sheep that received sodium sulfide creasingly recognized is associated with increased con-by gavage. 18 centrations of sulfur in water and/or feed and appears Only a small number of cattle subjected to n...

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Micronuclei induced in bone marrow erythroblasts by clastogenic chemicals are easily detected in peripheral blood. In mice treated with nitrogen mustard, 7,12 dimethylbenz(a)anthracene, or cyclophosphamide, the peak incidence of micronucleated polychromatic erythrocytes in peripheral blood was at least as great as the maximum incidence in bone marrow. In each case the peak incidence in blood occurred on the day following the peak incidence observed in bone marrow. Thus, for general genetic screening purposes, monitoring micronuclei in peripheral blood rather than in bone marrow smears provides at least equal sensitivity, offers greater simplicity in sample preparation and scoring, permits multiple sampling of treated animals, and may also facilitate automated scoring and human cytogenetic monitoring.

The plant toxin, 3-nitropropanoic acid, produced topographically and morphologically distinctive lesions in mice after daily intraperitoneal injections. In the lateral caudate-putamen there were bilateral and symmetrical lesions consisting of marked swelling and pyknosis of individual cells and processes in otherwise unaffected tissue. The appearance of transitional forms and the usual post-synaptic location of the swollen processes indicated that affected cells were neurons. A few mice exhibited a more diffuse spongy change in the lateral caudate-putamen that caused major architectural changes. In the globus pallidus, entopeduncular nucleus, and anterior substantia nigra pars reticulata there was fine spongy change of the neuropil that spared cell bodies, and was primarily due to swelling of dendrites. A third lesion pattern in myelinated tracts of the midbrain, medulla, and spinal cord consisted of adaxonal, intramyelinic cleft formation. Succinate dehydrogenase activities assayed in frozen brain sections and in isolated mitochondria were markedly reduced in intoxicated mice.