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Biomedical subjects

M Wyers

Publications and source records attributed to M Wyers.

32 records · Page 2Linked to original sources

[Nervous syndrome in sheep on the Ivory Coast. I. Epidemiological and clinical study, methods of diagnosis and treatment].

The ovine nervous syndrome in Côte-d'Ivoire is similar to the cerebrocortical necrosis (CCN) due to vitamin B1 deficiency. All classical symptoms of CCN were observed (locomotor ataxia with subsequent paralysis) and histological evidence for polioencephalomalacia was given. However, the circumstances for occurrence of the disease are very different in the two cases, i.e. CCN is a disease encountered in young fattening ruminants in developed countries while the ovine nervous syndrome is mainly observed in Côte-d'Ivoire during the dry season when pastures become sparse and dry and when the feed supply is insufficient. Thus, the main cause, which is rather univocal, is a sudden decrease in the nutritive value of the diet, but the accurate etiopathogenesis of the disease has not yet been determined. In a flock where 10-30% of the animals are ill, the mortality may reach 80-90%. No classical biochemical assays were specific enough to establish a precise diagnosis of the nervous syndrome. However, it should be pointed out that the CK (creatinine kinase) values very regularly rose and that the ASAT (aspartate aminotransferase) values were high in 75% of the cases. In the present African field conditions, the precise diagnosis is based on the efficiency of the vitamin B1 treatment and, for the dead animals, on the histological analysis of the brain.

Animals↗

[Analytical study of the locomotion of the meat turkey cock. Comparison between sound turkeys and turkeys with locomotor problems].

A comparative locomotion analysis of healthy and lame male commercial turkeys was carried out. Walking turkeys were filmed from both right and left lateral views. Video films were analysed. The coordination and the succession of hind limb movements were studied with time and space components. The gait of healthy turkeys was a walk with perfectly symmetrical and repeatable hind limb movements. All lame turkeys' movements showed abnormalities in space-time coordination. These abnormalities were bilateral but non-symmetrical, intermittent, and non-systematic. Their intensity increased with increase in the degree of clinical handicap. However, in all lame turkeys, the degree of an abnormal tibial movement was observed, ie a shorter amplitude of forward movement with variable intensity.

Animals↗

Hematological parameters and visceral lesions relationships in rabbit viral hemorrhagic disease.

Twenty rabbits were inoculated with a suspension of Viral Hemorrhagic Disease virus. Hemostatic functions were assessed every sixth hour from 6 to 60 hours post-inoculation. Tissue samples obtained at the same intervals allowed the study of the development of lesions throughout the experiment. Biological signs of Disseminated Intravascular Coagulation (DIC) were detected on and after 30 h post-inoculation and consisted of prolonged One Stage Prothrombin Time and Activated Partial Thrombin Time, the decrease of factors V, VII, and X and high levels of soluble fibrin monomer complexes and D-dimers. A reduction of thrombocyte numbers, heterophils and lymphocytes was associated. The close association of DIC and necrotizing hepatitis lesions suggested the hepatic lesions to be the most important DIC triggering factor. Other mechanisms are discussed.

Animals↗

Capripoxvirus disease in an Arabian oryx (Oryx leucoryx) from Saudi Arabia.

Lumpy skin disease caused by a capripoxvirus was observed in a captive-bred female Arabian oryx (Oryx leucoryx) at the National Wildlife Research Center, Taif, Saudi Arabia. Clinical signs included severe general depression with fever, anorexia, greater than 1,000 nodular cutaneous lesions and gradual recovery over 2 mo. The virus was found by electron microscopy and paired sera showed an increasing virus neutralization antibody titer against capripoxvirus. A serologic survey of the herd of 90 oryx showed a low prevalence (2%) of this infection. This report describes the first case of lumpy skin disease in an Arabian oryx.

Abortion, Veterinary↗

[Histomorphometric study of the superficial pectoral muscle of the turkey. Relationship with the meat discoloration syndrome].

Scallop discoloration affects about 30% of turkey carcasses, causing important economic losses. Histological and histomorphometric analyses of the superficial pectoral muscle were performed in order to show distinctive aspects of discolored scallops and predictive criteria for the phenomenon. Pectoral muscles of live male turkeys were biopsied 8 d before slaughter. Twenty four h after slaughtering, the same animals were classified into 2 distinctive classes by reflectometry (pale and dark muscles) and muscle samples were collected in each group. Superficial pectoral muscle was totally composed of type IIB, fast switch and glycolytic fibers. Pale and dark muscles exhibited no significant differences 8 d before slaughtering, but glycogen level was higher in pale muscles 24 h after slaughtering. These results do not support the current hypothesis of accelerated glycolysis and low ultimate pH to explain the meat discoloration syndrome in turkeys.

Animals↗

[Search for lesions caused by aflatoxin B1 poisoning in 3 industrial chicken farms on the Ivory Coast].

A systematic search for feed contamination by aflatoxin-B1 as well as for lesions indicating an acute or chronic aflatoxicosis was made in three groups of industrially raised hens in Côte-d'Ivoire. The contamination rates were low although they were 6 to 10 times higher than the official standards. No lesion due to an acute or chronic intoxication by aflatoxins was observed. However, the repeated intake of small amounts of aflatoxins might eventually have repercussions on the technics-economical performance either by a direct action of the toxin or via the development of an immune depression in the animals.

Aflatoxin B1↗

[Tibial dyschondroplasia in meat turkeys: morphometric study of its relationship with lameness].

The tibiotarsal bones from 1,084 15-week-old growing commercial male turkeys, half of which clinically lame, were examined for dyschondroplasia. Lesions were a cone of retained cartilage, confined to the postero-medial area of the proximal metaphysis of the tibiotarsus. Dense woven bone was present around the largest lesions associated with thickening of the diaphyseal cortex below the lesion. Length of abnormal cartilage varied from 0.1 cm to 5.3 cm. Width never exceeded 2.9 cm. Half of the affected turkeys showed unilateral localization of dyschondroplastic lesions. The percentage of damaged tibias was 54 per cent and the percentage of affected turkeys was more than 70 per cent. The incidence of dyschondroplasia was the same in lame and clinically healthy turkeys but, on average, lame turkeys exhibited longer lesions than clinically normal birds. The tibias of lame turkeys were more curved than the tibias of healthy ones as well in the anterio-posterior projection as in the latero-medial one. The latero-medial projection of incurvation was correlated with the length of dyschondroplastic lesions.

Animals↗

Histology and histomorphometry of the tibia growth in two turkey strains.

Qualitative and quantitative histological methods on decalcified and undecalcified specimens were used for comparing the linear and radial growth of the tibia in two turkey strains: a light strain, Betina, without leg problems and a heavy strain, Maxiboul, with leg problems. Groups of 10 clinically healthy male turkeys of each strain were studied at 2, 6, 8, 16, and 20 weeks of age. Three histomorphometric parameters of longitudinal growth were quantitated in the proximal growth plate and metaphysis. These were: height of the proliferative zone, density of ossification buds (metaphyseal sprouts), and volume of metaphyseal trabecular bone. Four histomorphometric parameters of radial growth were quantitated in the diaphysis. These were cortical thickness, active zone/total surface, density of maturing osteons in the active zone, and bone apposition rate at the maturing primary osteons level. The results showed some evidence for factors predisposing to leg problems in the Maxiboul strain. At 8 weeks, the Maxiboul strain had a lower ossification bud density (13.1/mm2 vs. 20.7/mm2; P less than .05) and a lower metaphyseal trabecular bone volume (16.4% vs. 22.0%; P less than .05) when compared to the Betina strain. No difference was detected in the cortical thickness of the diaphysis in the two strains except at 2 weeks of age (799 microns vs. 387 microns; P less than .001), despite the heavier weight of the Maxiboul strain.

Animals↗

Muscle lesions associated with dystrophin deficiency in neonatal golden retriever puppies.

Golden retriever muscular dystrophy (GRMD), a degenerative myopathy due to the absence of dystrophin, is genetically homologous to human Duchenne muscular dystrophy (DMD). Spontaneous death of GRMD neonates within the first 2 weeks of life occurs frequently. This report describes the microscopical muscle lesions that developed in 12 GRMD puppies aged 1-8 days of age, and makes a comparison with three normal age-matched siblings and two older GRMD dogs. Immunohistochemical methods were used to confirm dystrophin deficiency in GRMD puppies. Muscle lesions were assessed on sections stained with haematoxylin-eosin-saffron, Gomori's trichrome and alizarin red S, and their severity was graded semi-quantitatively. Muscle fibre types were determined immunohistochemically on the basis of the pattern of expression of developmental, slow and fast isoforms of myosin. Muscle lesions in the GRMD puppies were characterized by massive necrosis, affecting most muscles of the proximal limbs, trunk and neck at birth. Lingual lesions began to develop in utero, and respiratory muscles underwent terminal diffuse necrosis resulting in death from acute respiratory failure. However, GRMD puppies do not invariably die in the neonatal period. Muscle in 2-month-old GRMD dogs showed signs of regeneration (immunohistochemical immaturity of muscle tissue), which suggested that all GRMD dogs suffer from massive post-natal myonecrosis, whether fatal or not. Muscle lesions in neonates consisted mainly of hyalinization, hypertrophy, calcification and necrosis, followed by regeneration. Such "phase I" lesions due to the absence of dystrophin are found in all species in which dystrophin deficiency has been described (human beings, dogs, cats and mice), whereas the endomysial fibrosis and myofibre atrophy found in 2-month-old GRMD dogs constituted "phase II" lesions, which are specific to GRMD and human DMD.

Animals↗

Cerebral primitive neuroectodermal tumour in a heifer.

A primitive neuroectodermal tumour (PNET) replacing the thalamus was discovered in an 18-month-old Prim'Holstein heifer. Microscopical examination of the tumour showed large sheets of densely packed cells with occasional Homer-Wright and perivascular rosettes. Neoplastic cells were small with ill-defined borders, scant cytoplasm and ovoid, irregularly shaped nuclei. Immunolabelling was positive for vimentin and neuron-specific enolase, in agreement with previous reports of PNETs in human beings and animals. This appears to be the first report of cerebral PNET in cattle.

Animals↗

Late clinical expression of lameness related to associated osteomyelitis and tibial dyschondroplasia in male breeding turkeys.

A sudden outbreak of lameness related to transport stress is described in a flock of male breeding turkeys. Most of the affected turkeys exhibited obvious unilateral leg disorders. All were affected with tibial or metatarsal dyschondroplasia with at least one lesion associated with a large focus of necrosis. By histological examinations, bone lesions showed the typical feature of osteomyelitis. The inflammatory bone lesions appeared at only single isolated sites and were always associated with obvious sequestra of dyschondroplastic retained cartilage. Osteomyelitis seems to be an unexpected acute complication of previous dyschondroplasia in relation with different breeding stress situations. The resulting pain of the associated lesions could be the main cause of clinical expression of lameness. The pathogenesis of the phenomenon remains uncertain.

Animals↗