SUMMARY Caecal fluid samples collected 8 and 24 hours after carbohydrate overload were quantitatively compared to control samples in terms of aerobic and anaerobic bacteria. Concomitant increases in lactic acid‐producing bacteria and decreases in Gram negative bacteria were substantiated during the onset of acute laminitis. Progressive decreases in caecal fluid pH were also quantitated. Although endotoxin assays of caecal fluid and blood were not done, the caecal flora changes suggest its presence during the onset of acute laminitis. RÉSUMÉ Des échantillons de fluide coecal recueillis 8 et 24 heures apràs une surcharge digestive en hydrates de carbone furent comparés à des échantillons témoins pour apprécier les modifications de la flore aérobie et anaérobie. On constata une augmentation des bactéries productrices d'acide lactique et une diminution des bactéries Gram—avec installation des signes de fourbure aigue. Une diminution progressive du Ph du liquide coecal fut également remarquée. On ne contrôla point la présence d'antoxines dans le liquide coecal ni dans le sang. Mais les variations de la flore coecale laissent penser à l'existence de telles toxines au début de la fourbure aigue. ZUSAMMENFASSUNG Blinddarminhalt wurde 8 und 24 Stunden nach Kohlenhydratüberfütterung entnommen und quantitativ verglichen mit Kontrollproben (Zahl der aeroben und anaeroben Bakterien). Beim Eintritt einer akuten Hufrehe kommt es gleichzeitig zu einer Vermehrung von Lactat‐produzierenden Bakterien und zu einer Verminderung von Gram‐negativen Keimen. Ein zunehmender Abfall des pH im Blindarminhalt konnte ebenfalls quantitativ erhärtet werden. Obgleich Endotoxinbestimmungen in der Blinddarmflüssigkeit und im Blut nicht vorgenommen werden konnten, kann das Vorhandensein von Endotoxin aufgrund der Veränderungen der Flora beim Eintritt einer akuten Rehe vermutet werden.

Summary Thirteen (65 per cent) of 20 horses subjected to carbohydrate overload developed Obel Grade 3 lameness within 56 h. Increases in plasma endotoxin from control levels of less than 0.1 ng/litre to values ranging from 2.4 to 81.53 ng/litre were measured in 11 (85 per cent) of 13 horses during the onset of Obel Grade 3 lameness. Obel Grade 3 lameness was associated with rises in plasma Gram‐negative endotoxin levels in 11 (92 per cent) of 12 horses. Two peak increases separated by 16 h were verified in five (45 per cent) of 11 horses that exhibited both endotoxaemia and Obel Grade 3 lameness. The first peak occurred, on average, at 32 h and (he second peak at 48 h post overload when only one peak was measured, this occurred in four horses at the average time of 24 h whereas in another three horses only a 48 h or 56 h peak was detected after carbohydrate overload.

The role of Campylobacterjejuni in the pathogenesis of proliferative ileitis in Syrian hamsters was evaluated with monoclonal antibodies of different specificities. Monoclonal antibodies were produced with two different specificities: one for all members of the genus Campylobacter tested (antibody 8322-2E6) and one for C. jejuni and Campylobacter coli (antibodies 841-2A11, 841-4C6, and 841-5B1). Ileal sections from healthy hamsters, from hamsters with naturally occurring proliferative ileitis, and from hamsters with experimentally induced proliferative ileitis were examined by using fluorescein isothiocyanate-labeled, Campylobacter sp.-specific 8322-2E6 and tetramethylrhodamine isothiocyanate-labeled C. jejuni-C. coli-specific 841-2A11 for direct duallabeling immunofluorescence. Organisms which stained with the C. jejuni-C. coli-specific monoclonal antibody were observed in the ileal lumens and along the distal tips of the villi of hamsters with either experimentally induced or naturally occurring proliferative ileitis. In contrast, organisms identified by the Campylobacter sp.-specific monoclonal antibody were present deep within the villus lumens and crypts and intracellularly within the apical portions of the epithelial cells. No organisms stained with the C. jejuni-C. coli-specific monoclonal antibody were observed in ileal sections from control hamsters; an occasional intracellular organism stained with the Campylobacter sp.-specific monoclonal antibody was observed in 2 of 10 control hamsters. Thus, at least two immunologically distinct patterns were identified in ileal sections from hamsters with proliferative ileitis. On the basis of these results, we conclude that the organism seen intracellularly in ileal sections from hamsters with proliferative ileitis is a member of the genus Campylobacter but that it probably is not C. jejuni or C. coli.

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