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Biomedical subjects

K Nielsen

Publications and source records attributed to K Nielsen.

346 records · Page 20Linked to original sources
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A study of tail tip necrosis in young fattening bulls on slatted floors.

A questionnaire sent to 78 producers revealed that tail tip necrosis was seen only in units with fattening bulls housed on slatted floors. Out of 43 such units, 20 (46.5 per cent) reported that tail tip necrosis was a herd problem. All 43 herds were visited, owners were interviewed and housing and management data recorded. It is concluded that tail tip necrosis is a multifactorial disease. The initial lesion is caused by tramping, but the following factors are essential in the development and severity of the disease, i) slatted concrete floors, ii) close confinement, iii) hot season and iv) body weight above 200 kg. The stocking density (expressed as kg bodyweight per square meter pen) was significantly higher in problem herds (210 kg/m2) than in control herds (165 kg/m2). There was a close relationship between high environmental temperature and tail tip necroses. The majority of incidents occurred during the warm season (May through September), very few cases were seen during the colder months. The general morbidity and mortality rates were significantly higher in problem herds than in control herds. Microbiology of affected tails revealed mixed infections in most cases, with Corynebacterium pyogenes and Bacteroides melaninogenicus as the most frequently isolated organisms. Principles of treatment and prevention are discussed. There is evidence to assume that a 10-20 per cent reduction in stocking density could be an efficient prophylactic measure.

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PubMedDate not supplied

Electrocardiography in the horse. (A report of findings in 138 horses).

Over a period of approx. 3 years, electrocardiograms (ECG) were recorded from 138 horses referred as patients to the Medical Clinic. Of these, 22 horses (approx. 16 per cent) has ECG alterations. The 22 ECG's revealed a total of 29 ECG abnormalities. The most frequent ECG alteration was incomplete AV block, that was seen in 9 horses (31 per cent of the ECG abnormalities). Abnormal (i.e. broad, tent-like and, sometimes, inverted) T waves and deviations of the ST segment were seen each in 5 ECG's from 7 horses, 3 of which had both abnormalities which were associated with severe underlying disease (colic, enteritis, pneumonia, strangles a.o.). Premature ventricular beats were seen in 3 horses, two of which had serious cardiovascular dysfunction whereas the third showed no signs of cardiac disease. Atrial fibrillation was observed in two horses. Both were treated with chinidine sulphate but a conversion to sinus rhythm was not achieved in either case. Other ECG abnormalities observed in the study were, parasystole (1 horse), sinus arrhythmia (2 horses), sinoatrial block (1 horse) and wandering pacemaker (1 horse). Each abnormality is discussed with regard to its clinical significance and diagnosis. Cardiac murmurs were detected on auscultation of 26 horses (approx. 19 per cent). The murmurs in 15 horses were short and faint sounds most of which were diastolic. They were considered of no importance. Eleven horses, on the other hand, had distinct, loud (grade 4 or 5), holosystolic or holodiastolic murmurs that were considered pathological. Eight of these horses had actual signs of cardiac disease. Cardiac vector distribution in patients with ECG abnormalities or murmurs showed no systematic differences from vectors in horses showing no cardiac abnormality.

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