ABSTRACT
Continuous muscle fibre activity was observed in a crossbred dog, a Yorkshire terrier, a border collie and three Jack Russell terriers. The clinical signs consisted of episodes of generalised myokymia which developed into muscle stiffness and delayed muscle relaxation and generally led to the dogs collapsing into lateral recumbency. These episodes were preceded by intense facial rubbing in three of the dogs, and were associated with severe hyperthermia in five of them. All three Jack Russell terriers showed continuous ataxia. The dogs had above normal activities of aspartate aminotransferase, alanine aminotransferase and creatine kinase, but their cerebrospinal fluid was normal. Myokymic discharges were observed by electromyography in two of the dogs. Two of them were treated with membrane-stabilising agents, with variable results.
Subject(s)
Dog Diseases/physiopathology , Myokymia/veterinary , Animals , Anticonvulsants/therapeutic use , Dog Diseases/therapy , Dogs , Female , Fever/veterinary , Isaacs Syndrome/veterinary , Male , Muscle Fibers, Skeletal/physiology , Myokymia/physiopathology , Myokymia/therapyABSTRACT
Three- to four-week-old, just-weaned piglets were infected with transmissible gastroenteritis (TGE) virus and the next day with K88ac+ enterotoxigenic Escherichia coli (ETEC). Histological examination of caudal jejunum and ileum of piglets killed 2-3 days after virus challenge (1-2 days after ETEC infection) revealed severe villus atrophy especially in the jejunum compared with controls (P less than 0.05). Four-5 days after TGE virus infection villus length increased and after 7 days it was near normal. Villi scraped from jejunal and ileal mucosa of the piglets were incubated in vitro with K88ac+ E. coli and the number of bacteria adhering to 250 micron villus brush border was counted. Attachment of bacteria to villi of piglets killed 2-3 days after TGE virus infection was significantly decreased in comparison with adhesion to villi of non-infected piglets or of piglets killed 7 days after the virus infection. Correlation between in vitro adhesion and villus height was 0.6649 (P less than 0.001). The results suggest that the experimentally-induced villus atrophy was attended with a temporarily diminished susceptibility of villus enterocytes to adhesion of K88ac+ E. coli.
Subject(s)
Escherichia coli Infections/pathology , Intestine, Small/ultrastructure , Animals , Animals, Newborn , Atrophy , Escherichia coli Infections/veterinary , Intestine, Small/microbiology , Microvilli/ultrastructure , SwineSubject(s)
Endotoxins/pharmacology , Escherichia coli , Hemodynamics/drug effects , Swine/physiology , Animals , Female , Infusions, IntravenousABSTRACT
Clinical and pathological data of a recently discovered neurological disorder in young calves were studied. The symptoms were those of a paralysis of the nervus facialis and a dysfunction of the nervus vestibulocochlearis. Macroscopically, space occupying lesions were found at the roots of these two cranial nerves and in some cases further on their course into the os petrosum. On histological examination, these legions contained multiple nodules with mainly histiocytic cells, some plasma cells and multinucleated giant cells. Around these nodules, dense bands of connective tissue with fusocellular fibroblasts, some plasma cells and small blood capillaries were present. The nodular lesions were usually in close contact with the nerve. Ultrastructurally, a variety of cells, predominantly histiocytes and some plasma cells, were seen next to Schwann cells which contained degenerating axons.
Subject(s)
Cattle Diseases/pathology , Cranial Nerve Diseases/veterinary , Cranial Nerves/pathology , Disease Outbreaks/veterinary , Facial Paralysis/veterinary , Granuloma/veterinary , Animals , Belgium , Cattle , Cattle Diseases/epidemiology , Cattle Diseases/etiology , Cranial Nerve Diseases/pathology , Facial Nerve/pathology , Facial Nerve Diseases/pathology , Facial Nerve Diseases/veterinary , Facial Paralysis/epidemiology , Facial Paralysis/etiology , Facial Paralysis/pathology , Female , Granuloma/etiologyABSTRACT
Forty-two cases of canine pneumonia were examined for the presence of canine distemper virus. For that purpose canine distemper virus inclusion bodies were located. The histopathological lesions were related to the presence of canine distemper antigen, as demonstrated with an immunoperoxidase technique. This technique was more sensitive for detecting canine distemper infection in lung tissue than was the study of inclusion bodies. Attention was also paid to combined infection with canine adenovirus and Bordetella bronchiseptica.
Subject(s)
Distemper/diagnosis , Dog Diseases/diagnosis , Inclusion Bodies, Viral/ultrastructure , Lung/pathology , Pneumonia, Viral/veterinary , Adenoviridae Infections/complications , Adenoviridae Infections/diagnosis , Adenoviridae Infections/veterinary , Animals , Bordetella Infections/complications , Bordetella Infections/diagnosis , Bordetella Infections/veterinary , Bronchopneumonia/complications , Bronchopneumonia/diagnosis , Bronchopneumonia/veterinary , Distemper/complications , Dogs , Immunoenzyme Techniques , Methanol , Phenylhydrazines , Pneumonia, Viral/complications , Pneumonia, Viral/diagnosis , RabbitsSubject(s)
Adenoviridae Infections/veterinary , Dog Diseases/pathology , Pneumonia/veterinary , Adenoviridae/ultrastructure , Adenoviridae Infections/microbiology , Adenoviridae Infections/pathology , Animals , Dog Diseases/microbiology , Dogs , Lung/microbiology , Lung/pathology , Microscopy, Electron , Pneumonia/microbiology , Pneumonia/pathologyABSTRACT
Thirty-two horses were examined with a history of poor performance and unthriftiness several months after the ingestion of feed containing monensin sodium. Cardiac abnormality was diagnosed in 8 cases and suspected in 4 others. Necropsy examinations were performed on 6 cases with marked clinical symptoms and evidence of circulatory failure was found. Marked cardiac myopathy and fibrosis was a consistent feature. It is concluded that ingestion of monensin sodium by horses may cause either acute death or delayed cardiac circulatory failure as a result of specific cardiac myodegeneration.
