Atrial fibrillation associated with central nervous symptoms and colic in a horse: a case of equine cardiomyopathy.

A 18-year-old Dutch Warmblood mare was referred for colic. Upon arrival, lethargy, blindness, head pressing, ataxia, and circling were the main clinical signs. On rectal examination a hard mass and oedema around the cranial mesenteric artery were palpated. Plasma liver enzyme activities and the ammonia level were elevated. Atrial fibrillation with a pulse frequency of 36-52 beats per minute was noticed. On both sides a holosystolic murmer with the maximum intensity on the right side could be auscultated. Postmortem examination revealed eccentric hypertrophy of the right atrium and a pale spotted myocardium, most prominently of the right ventricle, with secondary venous congestion of the azygos and mesenteric veins. The liver changes were indicative of chronic congestion. Despite the normal pulse rate, it appeared that congestive heart failure due to cardiomyopathy, was responsible for the presenting symptoms of this patient.

[Neurodegenerative disorders of the central nervous system in horses]. / Neurodegeneratieve aandoeningen van het centrale zenuwstelsel bij het paard.

The most important neurodegenerative diseases of the horse are reviewed. In addition to the literature, neurodegenerative diseases occurring in patients (horses, Mongolian Przewalski-horses, and two zebras) referred to the Utrecht Veterinary Faculty are mentioned. Neurodegenerative diseases described are: I. ataxia associated with: A/ static stenosis, B/ dynamic stenosis, C/ lesions at various locations in the central nervous system, D/ equine herpesvirus infections, E/ equine degenerative myelo-encephalopathy, or F/ cerebellar abiotrophy; II. equine motor neuron disease; III. grass sickness or equine dysautonomia; IV. postanaesthetic myelomalacia; and V. equine leuko-encephalomalacia. The patient descriptions show, that mixed forms of some of the differentiated diseases can be diagnosed. Little is known with certainty about the aetiology of the neurodegenerative lesions found. In some patients vitamin E may play a role, possibly in combination with other factors. A mycotoxin known to interfere with myelin metabolism is involved in leuko-encephalomalacia.

[Narcolepsy in horses]. / Narcolepsie bij het paard.

Narcolepsy is an incurable non-progressive disease of the central nervous system. In humans, narcolepsy causes excessive drowsiness during the day (sometimes a sleep-attack occurs), cataplexy (sudden loss of muscle tone), hallucinations, and sleep paralysis. In the horse and other mammals cataplexy is the most frequently observed symptom. Excessive drowsiness can occur but is harder to observe. Cataplexy is caused by a fragmentation of the REM sleep. The etiology of narcolepsy is still subject to debate, partly because normal sleeping patterns are poorly understood. In humans and certain breeds of dogs a hereditary background has been demonstrated. In Shetland ponies the disease runs in certain families. The role of trauma and infection is the subject of debate. Cataplexy (which can be induced by physostigmine injection) confirms the diagnosis. Several drugs are available for the treatment of narcolepsy in humans. However there are a few data on the results of treatment of narcolepsy in the horse.

Pasteurella haemolytica leukotoxin enhances production of leukotriene B4 and 5-hydroxyeicosatetraenoic acid by bovine polymorphonuclear leukocytes.

The influence of the leukotoxin of Pasteurella haemolytica on the generation of arachidonic acid metabolites by bovine polymorphonuclear leukocytes (PMNs) was investigated. PMNs released 5-, 12-, and 15-hydroxyeicosatetraenoic acids (5-, 12-, and 15-HETE) and leukotriene B4 (LTB4) upon stimulation with arachidonic acid. The leukotoxin preparations dose dependently enhanced the release of the 5-lipoxygenase products 5-HETE and LTB4 in arachidonic acid-stimulated PMNs, whereas the release of 12- and 15-HETE was not affected. The enhanced release of LTB4 and 5-HETE was not due to a decreased cellular retention of the 5-lipoxygenase products. In addition, leukotoxin preparations by themselves were also able to induce LTB4 and 5-HETE production in the absence of exogenous arachidonic acid. Generation of 5-lipoxygenase products by PMNs stimulated by leukotoxin may represent an important cellular event that occurs during infections with P. haemolytica.

[Cecum amputation in a blond d'Aquitaine bull]. / Caecumamputatie bij een blonde d'Aquitaine stier.

A caecal torsion of 720 degrees was diagnosed in a one-and-a-half-year-old blonde d'Aquitaine bull. A partial amputation of the caecum had to be performed. The diagnosis and surgery of this case are described against the background of the usual dilatations and rotations of the caecum and ansa proximalis.

Aujeszky's disease in horses fulfils Koch's postulates.

Aujeszky's disease virus was isolated from the brain of a horse which had shown severe neurological signs, including excessive sweating, muscle tremors and periods of mania. Pathological examination revealed a non-suppurative meningoencephalitis. The virus was propagated in cell culture and inoculated into the conjunctiva and nostrils of two ponies. The ponies developed fever seven days after inoculation and subsequently started to behave abnormally, showing severe neurological signs on the ninth day after inoculation. One pony became excited and the other was depressed. One pony died on the ninth day after inoculation and the other was euthanased on the 10th day. Both ponies had a significant increase in serum antibody titre against the virus. The virus was recovered from several parts of the brains and the eyes of the ponies. Aujeszky's disease in horses therefore fulfils Koch's postulates. Although horses do not appear to be very susceptible to the virus, Aujeszky's disease should be included in the differential diagnosis of horses with fatal or transient neurological signs of disease in areas where the virus is endemic.

Aujeszky's disease in a horse.

A horse with neurological signs and severe meningoencephalitis caused by Aujeszky's disease is described. The diagnosis was established by immunohistochemistry, DNA-in situ hybridization and serological tests. Aujeszky's disease virus antigen and Aujeszky's disease viral DNA were detected in neurons of the cerebrum. In the serum of the horse antibodies against Aujeszky's disease virus were detected in a virus neutralization test, in a blocking ELISA which specifically detects antibodies against the glycoprotein I (Ig) of the virus, in an indirect double sandwich ELISA and with colloidal gold immunoelectron microscopy which detects antibodies directed against the envelope and nucleocapsid of the virus. Intranasal infection of two points with a high dose of Aujeszky's disease virus caused very wild and transient signs. Although the experimental infection induced virus neutralizing antibodies, it failed to induce gI specific antibodies.

The effect of stress on host defense system and on lung damage in calves experimentally infected with Pasteurella haemolytica type A1.

This paper describes the influence of stress, immediately before a massive inoculation of a log-phase P. haemolytica A1 culture in brain-heart-infusion broth by fiberoptic bronchoscopy in 5 months old conventional calves. Differences in phagocytic cell function and numbers, lung function and lung tissue damage between stressed and non-stressed, infected calves were studied. Compared with the non-stressed calves before infection, the superoxide generation by blood polymorphonuclear leucocytes of the stressed animals was markedly reduced immediately after a 2 hours stress period, but it recovered within 3 days. The total numbers of phagocytic cells, harvested from lung lavage fluid 3 days after inoculation were twice as high in the non-stressed calves than in the stressed calves. In contrast, no differences in pulmonary lesions and functions were found between stressed or non-stressed calves. The role of several stress factors on infiltration and metabolic response of polymorphonuclear leucocytes in P. haemolytica infections and the effects of bacterial endotoxin and leukotoxin on alveolar and vascular injury are discussed.

Pulmonary lesions induced by a Pasteurella haemolytica cytotoxin preparation in calves.

Intrabronchial instillation of a Pasteurella haemolytica type A1 crude cytotoxin preparation in calves resulted in pulmonary gross and microscopic lesions comparable to spontaneous and experimental pasteurellosis. In the acute stage of the lesion electronmicroscopy revealed intravascular accumulation, degeneration and fragmentation of leukocytes in the interalveolar septa. Secondary thrombus formation and increased vascular permeability resulted in alveolar flooding, fibrin deposition, extravasation of erythrocytes and loss of alveolar epithelium. No cytotoxicity was observed for the tracheal (in vitro) and bronchial epithelium (in vivo). The pathogenesis of the vascular lesions and their significance for the development of the typical lesions of pneumonic pasteurellosis is discussed.

The effect of Pasteurella haemolytica cytotoxin on bovine polymorphonuclear leukocytes can be attenuated by beta-adrenoceptor antagonists.

It was investigated whether beta-adrenoceptor antagonists could disturb the interaction between cytotoxin preparations isolated from Pasteurella haemolytica and bovine polymorphonuclear leukocytes (PMNs). The toxicity of the cytotoxin preparation was evaluated by measuring the chemiluminescence response and the viability of the cells after incubation with the cytotoxin. No effect on cell viability was detected when PMNs were incubated with 63 micrograms cytotoxin per ml while the chemiluminescence response was diminished by approximately 30%. The beta-adrenoceptor antagonists alprenolol (10(-5) M) and propranolol (5 X 10(-7) - 5 X 10(-6) M) were able to attenuate this effect of cytotoxin on the chemiluminescence response of PMNs. It seemed unlikely that propranolol and alprenolol diminished the effect of cytotoxin on the chemiluminescence response of PMNs by their beta-adrenoceptor blocking potency because other beta-adrenoceptor antagonists used were without effect. Also, the membrane stabilizing characteristics of the beta-adrenoceptor antagonists used were probably not responsible for the diminished interaction between PMNs and the cytotoxin. Whether beta-adrenoceptor antagonists could be used in vivo to prevent or treat P. haemolytica infections in bovines remains to be examined.

Stress diminishes infiltration and oxygen metabolism of phagocytic cells in calves.

The influences of a stress situation on the phagocytic cell function before and after infection with Pasteurella haemolytica were measured in calves. No differences in phagocytic and metabolic activity of alveolar macrophages (AMs) were observed in vitro between cells isolated from stressed and nonstressed animals. The uptake of bacteria and the migration of polymorphonuclear leukocytes (PMNs) did not differ. However, the production of superoxide by PMNs isolated from stressed animals was significantly diminished as compared to control PMNs. The stressed and six of the nine control calves were then infected intrabronchially with P. haemolytica. Phagocytic cell function was again evaluated after three days. The lavage fluid obtained from the lungs of the infected animals contained about three times more PMNs and six times more AMs as compared to the lavage fluid of the control calves. However, the increase in phagocytic cell numbers was less by half in the calves infected after the stress period. No differences were detected in phagocytic and metabolic activity of PMNs and AMs among control, infected, and stressed and infected calves. However, the chemotactic activities of PMNs obtained from infected stressed and infected nonstressed animals were diminished as compared to control PMNs. In conclusion, the metabolic responsiveness of PMNs is diminished and the accumulation of phagocytic cells at a site of infection is reduced after a stress period.

Antibiotic levels in bovine lacrimal fluid after single application of ointments containing procaine benzyl penicillin plus dihydrostreptomycin; and benzathine cloxacillin.

The efficacy of an experimental slow-release formulation, containing procaine benzyl penicillin and dihydrostreptomycin, was investigated in a cross-over study with a cloxacillin eye ointment in 12 cows with clinically normal eyes. After a single topical application the therapeutic concentrations of penicillin were sustained for 48 to 92 hours and of cloxacillin for 32 to 48 hours. These long-acting ointments will simplify the successful treatment of painful eye disorders such as keratoconjunctivitis. A practical and non-irritant method for sampling tears is described.