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High winter mortality (28 per cent) in female Jersey calves (80 IU/l in healthy females aged 3-24 weeks, and correlated with serum aspartate transaminase (AST). Copper supplementation of total mixed rations during lactation was excessive (40-60 mg added Cu/kg DM) and reduced to 16-28 mg Cu/kg, but supplementation of milk replacer and creep feed (10 and 35 mg added Cu/kg DM, respectively) continued. The syndrome recurred two years later, and liver Cu remained high in casualties (13.6 ± 2.6) and culled cows (6.38 ± 2.38 mmol/kg DM) prompting withdrawal of all Cu supplements. Mortality remained low (6-9 per cent) thereafter. Three years after removal of all Cu supplements, six culled newborn were examined postmortem; five had normal liver Cu (4.5 ± 1.73), but a sixth had 11.65 mmol/kg DM. In live, healthy calves (1-6 months old) sampled at the same time, GLDH and AST increased with age to levels found five years earlier, indicating possible subclinical hepatopathy. Causative links between Cu supplementation, high calf mortality and hepatopathy are plausible, and reductions in Cu supplementation may prove beneficial in other dairy herds.

Comprehensive bacterial cultures were made on samples from 20 pigs that had died of porcine dermatitis and nephropathy syndrome after a short clinical illness. Eleven species of porcine bacterial pathogens and a range of commensal organisms were isolated. Pasteurella multocida was isolated from 16 of the 20 cases but the other pathogens occurred much less commonly. P. multocida was isolated from between one and five sites per case and from the tonsils, retropharyngeal lymph node or lungs in 14 of the 16 cases. Immunohistochemical investigations of kidneys from 30 cases of the syndrome (including the 20 cases in the bacteriological study) revealed P. multocida-specific staining in 26 of the cases, primarily in the renal tubular epithelial cells of the proximal convoluted tubules, but also in the glomeruli, in lesions of renal vasculitis and in the cytoplasm of interstitial mononuclear cells.

Investigations into the possible causes of colitis and typhlocolitis were carried out on 85 pig units in the United Kingdom between 1992 and 1996. Serpulina pilosicoli was identified most commonly, occurring as the suggested primary agent on 21 (25 per cent) of the units but forming part of mixed infections on another 23 (27 per cent) of the units, the main co-infections being Yersinia pseudotuberculosis (eight units), proliferative enteropathy (six units), Salmonella species (four units) or Serpulina hyodysenteriae (two units). 'Atypical' Serpulina species, S hyodysenteriae, Salmonella typhimurium, Y pseudotuberculosis and Lawsonia intracellularis (proliferative enteropathy) were the suggested primary agents on seven, six, four, four and three units, respectively. Various combinations of mixed infections involving the latter organisms and other possibly incidental agents were recorded on another 10 units. Investigations on a further six units failed to detect any recognised pathogens. On units where S pilosicoli was the suggested primary agent, pigs ranging between 20 to 40 kg (eight to 16 weeks of age), but occasionally up to 50 kg, had diarrhoea and grew poorly over a period of two to three weeks. The prevalence was estimated to be between 5 and 15 per cent in affected batches, with a mortality of approximately 1 per cent. The clinical signs usually developed seven to 14 days after the moving and mixing of pigs. At postmortem examination, affected pigs had liquid contents in their colon, which contained accumulations of mucus in some chronic cases. Gross and histological lesions of colitis were prominent in the mid-spiral region of the colon. In mixed infections with Y pseudotuberculosis, Salmonella typhimurium or S hyodysenteriae, lesions were more extensive and affected the caecum as well as the colon. In the colon, lesions of proliferative enteropathy were usually confined to the proximal half of the ascending spiral but mixed infection with S pilosicoli caused more extensive colitis. Mixed infections were reported to prolong the time taken for pigs to recover naturally and to have a more detrimental effect on growth rates than S pilosicoli infection alone. Despite the successful treatment of batches of pigs with tiamulin or lincomycin, S pilosicoli infection persisted as a chronic problem on many units, with diarrhoea and colitis in successive batches of pigs unless prophylactic medication was used.

Infections in pregnancy with Ureaplasma urealyticum have been associated with a wide range of adverse outcomes, such as early abortion, stillbirth, prematurity, and neonatal morbidity and mortality. Causality has been difficult to demonstrate secondary to the high prevalence of asymptomatic lower genital tract (LGT) colonization and culture data from inaccessible or potentially contaminated sites. Between 1985 and 1989, 2461 second-trimester genetic amniocenteses were evaluated at the cytogenetics section of the Children's Hospital Medical Center of Akron. All were cultured for the genital mycoplasmas: Mycoplasma hominis and Ureaplasma urealyticum. A total of nine patients were positive, all for Ureaplasma urealyticum, with one patient excluded because of subsequent therapeutic abortion. In addition, complete follow-up data, such as indication for amniocentesis, serum alpha-fetoprotein levels, gestational age at parturition, and outcome of pregnancy, were available on 86 Ureaplasma-negative (U-) patients during an approximate 2-year span within the time-frame of the study. This was in part due to physician response to a questionnaire sent after amniocentesis. Of the eight positive cultures, 100 per cent were associated with an adverse outcome, defined as fetal loss or premature delivery. This was significant compared with the U- group (p less than 0.001) with a more than eight times greater risk of adverse outcome. Six (75 per cent) resulted in spontaneous miscarriage within 4 weeks of amniocentesis and at less than 21 weeks' gestation. Two (25 per cent) delivered prematurely, with one (12.5 per cent) neonatal death at 24+ weeks. Histological examination of all eight placentae and the seven fetuses revealed a 100 per cent incidence of chorioamnionitis and pneumonia, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The therapy of equine chronic obstructive pulmonary disease (COPD) essentially entails minimising the horse's exposure to the aetiological antigens which are predominantly thermophilic actinomycetes and moulds occurring in hay and straw. This can be achieved, for example, by keeping affected horses permanently out of doors, or when stabled, using shredded paper, wood shavings or peat moss as bedding and feeding a complete cubed diet. There should be no supplementary hay feeding apart from dust-free vacuum-packed hay. Applying such measures generally allows horses to become asymptomatic in seven to 14 days. Bronchodilators and corticosteroids bring about a marked, but temporary, improvement and can be of value in the treatment of acute attacks. The use of oral bronchodilators in combination with environmental control measures may hasten the remission of clinical signs in affected horse. Inhaled sodium cromoglycate can be used prophylactically in asymptomatic horses to prevent the onset of COPD when unavoidable antigen exposure is anticipated.

A respiratory virus vaccination trial was carried out in a commercial calf-rearing unit with a history of virus pneumonia. The effects of vaccination on the incidence of virus respiratory disease and growth rate were assessed. Forty-four bought-in calves were allocated to groups and treated as follows: A, unvaccinated controls; B, intranasal temperature-sensitive infectious bovine rhinotracheitis (IBR) vaccine at three and 10 weeks; C, intranasal temperature-sensitive combined IBR and parainfluenza-3 (PI3) vaccine at three and 10 weeks; D, intranasal temperature-sensitive combined IBR and PI3 vaccine at three and 10 weeks plus live attenuated bovine respiratory syncytial (BRS) virus vaccine intramuscularly at seven, 10 and 16 weeks. Two outbreaks of virus pneumonia occurred, one at three to four months of age associated with BRS virus and the other at four to five months of age with PI3 virus. During these outbreaks the incidence of pneumonia was lower and the number of days of elevated temperature and the number of treatments were significantly less in groups vaccinated against the associated virus. Despite these findings there were no significant differences between the growth rates of the groups either during the outbreaks of virus pneumonia or during the 10 month period to slaughter.

The effects of environmental control on horses affected with chronic obstructive pulmonary disease was assessed by clinical examination and pulmonary function tests, ie, maximum change in intrathoracic pressure, tidal volume, minute volume, non-elastic work of breathing, dynamic compliance, inspiratory and expiratory flow rates and arterial blood gas analysis. A controlled environment (ie, bedding horses on shredded paper and feeding a complete cubed diet) caused symptomatic COPD affected horses to become asymptomatic within four to 24 days (mean +/- sd 8.4 +/- 4.8 days). When asymptomatic, their pulmonary function values did not differ significantly from those of normal horses, which indicates that the pathophysiological changes occurring in equine COPD are reversible. The time taken for horses to become asymptomatic correlated significantly with age, duration of illness and severity of disease as adjudged by the non-elastic work of breathing.

When stabled in a controlled environment, horses effected with chronic obstructive pulmonary disease (COPD) became clinically asymptomatic in 4 to 32 days (mean [+/-sd] 9.1 +/- 4.9 days), the time being influenced most by the severity of the disease judged on maximum intrathoracic pressure change (Max delta Ppl) and the age of the animal. Sodium cromoglycate, a drug widely used for prophylaxis of allergic respiratory disease in man, was administered by inhalation to 56 COPD-affected horses. The results showed that a linear response existed between the number of successive days treatment with this drug and the duration of remission of clinical signs of COPD while horses were exposed to natural antigen (poor quality straw bedding). Sodium cromoglycate given as a single daily dose (80 mg) on one day and on 4 successive days prevented clinical signs for mean 3.6 days and mean 24.3 days, respectively. These results indicate that prophylactic treatment with inhaled sodium cromoglycate is an effective method of controlling the clinical signs of COPD.

An abattoir survey on horses diagnosed as suffering from chronic obstructive pulmonary disease (COPD) on clinical grounds showed that the right ventricular wall thickness was not significantly different from that of normal horses. However, the weight ratio between the left and right ventricles was found to be significantly (P less than 0.001) different in COPD affected, compared with control, horses in a study of 17 physiologically and pathologically confirmed COPD cases, using ventricular weight measurements. No clinical evidence of right heart failure nor post mortem evidence of right heart dilatation was observed in any COPD affected animals. It is suggested that the low incidence and degree of cor pulmonale in equine COPD may be related to the reversibility of the pulmonary hypertension associated with this disease.

The aetiology, pathophysiological changes, pathology and clinical signs of the disease as presently understood are discussed. The condition appears to be a hypersensitivity of the respiratory system in some horses to poor quality hay and straw. Micropolyspora faeni is the chief agent identified in the northern part of the United Kingdom. In other locations, the chief agent is probably different. The principal changes are spasm of the airways and bronchiolitis of the small airways. Onset may be acute or insidious. The chief clinical signs are well known but the disease process is reversible if the source of the antigen is removed. In early cases, determination of increased maximum intrathoracic pressure changes and co-existent subnormal arterial oxygen pressure are the best objective confirmation of diagnosis. The same measurements may be made on asymptomatic horses if they have been challenged 4 to 5 h earlier by inhalation of the appropriate antigen, or even exposed to poor quality hay or straw. Other methods available to the clinician are discussed.

Subclinical mastitis caused by streptococcal infections affected 27 of 83 cows in a commercial dairy herd. Between three and six weeks after intramammary treatment of these cows with cloxacillin, 16 (59 per cent) of the treated cows developed acute clinical mastitis associated with Mycobacterium smegmatis. None of the untreated cows was affected. Infected quarters were moderately hypertrophied and fine clots were present in the milk for three to four weeks. No cows showed systemic signs of illness. Studies carried out over 12 months showed that infected cows shed M smegmatis for three to four months and affected quarters remained hypertrophied in all but one cow after 12 months. The mean milk cell count of affected quarters fell slowly from 4,850,000/ml in the acute stage to 810,000/ml five months later and 620,000/ml 12 months later, suggesting that the organism persisted in the udder. The estimated mean loss in lactation yield for cows with M smegmatis mastitis was 10.8 per cent. Losses were greatest when the hind quarters were involved (mean 28 per cent for cows with both hind quarters affected). Ten of the 16 affected cows were ultimately culled owing to serious reductions in yield.