Antibiotic pressure and nosocomial disease

Nosocomial infection control programs of various types have been implemented in human hospitals since the staphylococcal pandemic of the 1950s. The prevalence of hospital infections is expected to increase in veterinary medicine with the advent of sophisticated invasive monitoring techniques, lengthier patient hospital stays, and the widespread use of antimicrobial agents. In order to monitor and control nosocomial infection outbreaks, the hospital staff must make strategic measures a priority. We propose the establishment of a nosocomial infection control committee, especially at the larger teaching and referral centers, to oversee such activities as hospital and personnel hygiene protocols, patient handling, antisepsis of surgical and critical care instruments, and surveillance. We have described a hospital pharmacy antibiotic restriction policy similar to those used with success in several human hospitals. It is apparent that the careless use of antibiotics adds significantly to the emergence of resistant hospital microflora and predisposes hospitalized patients to nosocomial infections. Judicious use of antibiotics not only helps to curtail such risks and lower health costs but encourages the clinician to fully evaluate his or her therapeutic rationale. As with any new program, continued staff education is the paramount requirement for its success.     

Atresia of the nasolacrimal orifice in two thoroughbreds.

Two cases of bilateral atresia of the nasolacrimal orifice are described. The presenting sign was a persistent ocular discharge, clear in the one case and purulent in the other. Treatment by the creation of a fistula between the distal extremity of the blind ending duct and the nasal cavity was successful in both cases.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. I. Clinical profile of horses

Detailed physical and clinical examinations were performed on 26 Thoroughbred racehorses which were used subsequently in a series of studies to investigate the contribution of the pulmonary and bronchial arterial circulations to the pathophysiology of exercise-induced pulmonary haemorrhage (EIPH). Twenty-five of the horses had been retired from race training in Hong Kong during the 1984-85 season, all but four raced that season; one horse had been retired the previous season. The average number of races for the group that season was 4.1 +/- 2 with an average distance of 1502 +/- 216 metres, mean racing speed 15.5 +/- 0.5 metres/sec. Time from last race to necropsy was 177 +/- 155 days, range 12 to 572 days. All but one horse had a known history of either EIPH or epistaxis. Time from last recorded incident of expistaxis (17 horses) to necropsy was 156 +/- 141 days, range 12 to 513 days, with a longer interval since last recorded endoscopic observation of EIPH. Focal abnormal lung sounds were detected in the dorsocaudal lungfields on auscultation during rebreathing in three horses and six had tracheobronchial cytology consistent with previous episodes of pulmonary haemorrhage (haemosiderophages). No other characteristics which might have allowed separation of this group of horses from other Thoroughbred horses recently in race training were identified.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations

This study was initiated to determine if the extent and intensity of lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses could be predicted from thoracic radiographs. Sets of thoracic radiographs from 24 horses with varied histories of EIPH were subjectively coded for radiographic quality, and perceived extent and intensity of diffuse interstitial opacity by three radiologists who had no knowledge of the corresponding autopsy results. Codes assigned from radiographs for the chosen parameters were compared with coded estimates of lung surface staining assigned at post mortem and volume measurements of haemosiderin deposits and bronchial arterial neovascularisation recorded from lung slices in separate studies. The non-parametric Spearman rank correlation test was used to test for statistical significance. All radiographically coded estimates of lesion severity were positively correlated with post mortem measurements of actual lesion involvement, but only the correlation between coded estimates of lesion opacity versus haemosiderin deposits and bronchial artery neovascularisation were statistically significant (P less than 0.05). Correlations between radiographic codes for lesion extent versus haemosiderin deposits and neovascularisation were just beyond the level of significance (P greater than 0.05 less than 0.1). These findings indicate that there are graded, radiographically discernible increases in interstitial opacity related to actual lesion severity. However, under the conditions of the study, accurate prediction of lung pathology in individual cases based on radiographic criteria was precluded by the wide variance of the coded values. The authors believe that with good radiographic technique and careful criteria selection, satisfactory prediction of lesion severity in EIPH cases could be achieved.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VIII. Conclusions and implications

This paper reviews a series of clinical, post mortem and imaging studies on exercise-induced pulmonary haemorrhage (EIPH) performed on 26 Thoroughbred racehorses. Post mortem techniques included routine gross, subgross and histological examination; coloured latex perfusions of pulmonary and bronchial circulations; and microradiography and computerised tomography scans of lungs with contrast injected vasculature. The major lesions were multiple, separate and coalescing foci of moderately proliferative small airway disease accompanied by intense neovascularisation of the bronchial circulation. As a result of bronchial artery angiogenesis, the systemic circulation dominated the vascular supply of the air exchange structures in affected areas, producing an apparent left to right shunt. Extensive areas of sequestered haemosiderophages indicated previous haemorrhage from vessels apparently supplied by the bronchial arteries. Diffuse and focal parenchymal destruction and connective tissue reactions in affected areas were considered to be secondary to localised haemorrhage and macrophage-induced damage. The aetiology of EIPH was not determined, but the multifocal, small airway-centred lesions indicated that low grade bronchiolitis, possibly of viral origin, was a factor. Gravitational effects also appear to contribute to dorsal distribution of the lesions. The mild focal and subclinical lesions confined to secondary lobules are thought to evolve into the serious lung pathology observed in EIPH cases through the effects of localised hypoxia induced by maximal exercise and partial airway obstruction. Once initiated, a vicious cycle of increasing inflammatory damage and further local bleeding is set in motion.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. III. Subgross findings in lungs subjected to latex perfusions of the bronchial and pulmonary arteries

Latex was injected under pressure into bronchial and pulmonary arteries of the inflated lungs of Thoroughbreds and transverse sections taken to calculate the area of lesions resulting from exercise-induced pulmonary haemorrhage. Extensive areas of dense brown haemosiderin varying from 0 to 45 per cent of total lung volume were identified, predominantly in the dorsocaudal lungfields. Bronchial arterial proliferation appeared to have replaced the pulmonary supply in affected areas of the lung. Closely associated with the staining and bronchial arterialisation, there was widespread small airway disease. The most severely affected bronchioles contained thick gelatinous or mucous exudate or mucoid plugs and had grossly thickened walls. These lesions suggest that the source of haemorrhage in exercise-induced pulmonary haemorrhage is from alveolar capillaries anomalously supplied by the bronchial arterial circulation through the development of pathological shunts. Small airway disease is suggested as being of major importance in the pathogenesis of the disease and may have led to the initial proliferation of the bronchial circulation.